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LECTURES 


ON 


DISEASES  OF  THE  HEART 


DELIVERED    AT  THE 


College  of  Physicians  and  Surgeons,  New  York 


BY 


ALONZO  CLARK,  M.D.,  LL.D. 

Emeritus  Professor  of  the  Principles  a7td  Practice  of  Medicine,  Etc. 


BERMINGHAM  &  COMPANY 


28  Union  Square.  East 
NEW  YORK 


1884 


20  King  William  Street,  Stranq 
LONDON 


Copyright.  1884,  by  Bermingham  &  Co. 


He  lo  8  \ 

C  -5r4- 


CONTENTS. 


LECTURE   I. 

PAGE 

Heart  Sounds • 9 

LECTURE   IL 
Pericarditis • 3^ 

LECTURE   in. 
Endocarditis <> «     96 

LECTURE   IV. 
Myocarditis 116 

LECTURE  V. 
Hypertrophy  of  the  Heart.' 122 

LECTURE  VL 
Dilatation  of  the  Heart 132 

LECTURE  VIL 
Fatty  Degeneration  of  the  Heart 142 

LECTURE  VIII. 
Rupture  of  the  Heart.  0 150 

LECTURE   IX. 
Fibrous  Degeneration  of  the  Heart 156 


6  CONTENTS* 

LECTURE  X. 

PACK 

Heart  Clots..,   *** *...* I59 

LECTURE  XL 
Valvular  Disease • 163 

LECTURE   XIL 
Valvular  Disease  {continued) 179 

LECTURE   XIIL 
Prognosis  and  Treatment  of  Valvular  Disease 204 

LECTURE  XIV. 
Angina  Pectoris 216 

LECTURE  XV. 
Deformities  of  the  Heart 222 

LECTURE   XVL 
Functional  Diseases  of  the  Heart 235 

LECTURE   XVn. 
The  Effects  of  Certain  Drugs  on  the  Heart 242 


PREFACE. 


This  book  contains  the  substance  of  my  lectures  lipoil 
"  Diseases  of  the  Heart,"  delivered  at  the  College  of 
Physicians  and  Surgeons  for  many  years  past,  together 
with  reports  of  cases  collected  from  the  literature  of 
the  subject,  and  from  personal  observation. 

The  basis  of  the  work  being  a  course  of  didactic 
lectures,  the  style  is  colloquial,  and  though  it  may  not 
possess  that  rhetorical  rounding  which  is  the  offspring 
of  elaborate  revision,  it  is  given  to  the  profession  as  an 
exposition  of  the  views  which  I  have  inculcated  during 
the  many  years  in  which  I  have  been  a  teacher. 

New  York,  March  21,  1884. 


DISEASES  OF  THE  HEART. 


LECTURE  I. 

HEART     SOUNDS 


I  WILL  first  make  a  few  preliminary  remarks  upon  what 
is  essential  to  an  understanding  of  endocarditis  and  val- 
vular diseases  of  the  heart. 

Here  you  observe  a  heart,  a  very  large  one,  laid  open. 
You  observe  that  the  inner  surface  of  this  cavity  is  lined 
by  a  smooth,  shining  membrane.  This  is  called  the  en- 
docardium, a  serous  membrane  somewhat  analogous  to 
that  which  lies  upon  the  outside  of  the  heart.  This  mem- 
brane lines  all  these  muscles,  protecting  the  muscular 
structure  entirely  from  contact  with  the  blood.  This 
same  lining  membrane  is  to  be  found  in  every  cavity  of 
the  heart,  and  it  is  continuous  in  a  certain  way  from  one 
to  the  other. 

Now  observe  how  a  valve  is  made.  Here  is  the  semi- 
lunar valve  of  the  aorta.  If  you  will  examine  this  you 
will  see  that  the  tissue  is  absolutely  continuous  from  the 
wall  of  the  ventricle  on  to  this  valve.  Follow  it  on  a  lit- 
tle further ;  it  doubles  down  upon  this  valve,  and  then 
from  there  is  reflected  off  on  to  the  base  of  the  aorta. 
Well,  a  valve  of  the  heart  is  made,  then,  of  a  duplication 
of  the  lining  membrane,  of  a  duplication  of  the  endocar- 
dium.    The  valve  is  closed  when  it  lies  against  the  aorta, 


to  HEART  SOUNDS* 

and  you  can  then  hardly  see  how  it  is  constructed ;  but 
open  it  and  you  see  it  is  the  same  Hning  membrane  of  the 
ventricle  which  doubles  down  to  the  bottom  of  this  valve 
and  then  passes  off,  without  being  broken,  into  the  great 
vessel. 

The  mitral  valve  is  made  in  the  same  way,  but  the  lin- 
ing membrane  of  the  ventricle  goes  down  upon  the  pos- 
terior face  of  the  mitral  valve,  doubles  upon  itself,  and 
goes  back  into  the  auricle.  To  this  valve  are  attached  a 
considerable  number  of  little  cords  that  go  down  into  the 
ventricle  and  are  there  attached  to  what  are  called  the 
fleshy  columns.  The  endocardium  is  no  less  continuous 
for  that  reason.  Indeed,  it  doubles  upon  these  cords, 
and  covers  them.  Each  valve,  in  each  part  of  the  heart, 
is  made  in  this  same  way,  but  there  is,  however,  a  little 
more  to  each  of  these  valves.  There  is  a  fibrous  struct- 
ure in  the  middle  of  them — you  may  say  a  skeleton  ; 
something  like  the  frame  of  a  house  before  there  are  any 
boards  or  plaster  put  upon  it.  The  fibrous  tissue  of  the 
valve  lies  between  two  folds  of  membrane.  Now,  it  hap- 
pens that  in  endocarditis  the  aortic  or  the  pulmonary 
valve,  is  most  likely  to  show  the  results  of  inflammatory 
action. 

But  the  point  I  want  to  impress  upon  you  is  the  way 
the  blood  circulates  through  the  heart,  and  what  the  heart 
does  in  the  course  of  the  circulation  of  the  blood  through 
it. 

Suppose  the  blood  is  coming  in  from  the  lung.  In  the 
period  of  rest  the  left  auricle  is  being  distended  by  the 
blood  coming  in  from  the  lung.  The  contraction  of  the 
heart  begins  in  the  auricle,  and  almost  instantly  spreads 
to  the  ventricle.  The  result  of  this  little  contraction  of 
the  auricle  before  the  ventricle  begins  to  contract  is  to 
send  a  little  more  blood  into  the  ventricle,  or  perhaps  to 
send  a  portion  of  it  backward,  because  there  is  no  valve 


HEART  SOUNDS.  11 

which  Will  prevent  its  going  either  way.  Then  the  left 
ventricle  contracts.  What  becomes  of  the  blood  ?  It 
goes  into  the  aorta,  and  if  there  is  anything  to  obstruct  it, 
it  may  make  a  noise,  which  is  not  normal,  and  which  is 
known  as  a  bruit  or  murmur.  Then,  when  you  have  a 
murmur  produced  at  the  base  of  the  heart  when  the  ven- 
tricle contracts  it  is  produced  by  an  obstruction — it  may 
be  a  narrowing  of  the  vessel  at  the  valves.  Now,  what 
else  takes  place  when  the  ventricle  contracts  ?  If  there  is 
any  way  for  the  blood  to  get  out  except  the  normal  it  will 
take  that,  as  well  as  its  natural  way.  Suppose  the  mitral 
valve  is  insufficient  ;  suppose  it  be  diseased  in  such  away 
that  it  cannot  close  perfectly  ;  what  is  there  to  prevent  the 
blood,  when  the  ventricle  contracts,  going  back  over  the 
very  track  it  came  ?  Nothing  in  the  world.  Well,  then, 
when  this  mitral  valve  is  insufficient,  and  you  get  a  mur- 
mur from  it,  it  will  be  when  the  ventricle  contracts  :  this 
is  regurgitation.  When  in  systole,  or  contraction  of  the 
ventricle,  there  is  a  murmur  at  the  aortic  opening,  it  is 
due  to  obstruction. 

Now,  suppose  this  aortic  valve  to  be  so  far  diseased,  so 
far  narrowed  and  shortened,  that  the  three  different  por- 
tions of  the  valve  cannot  meet  in  the  miiddle  of  the  artery, 
and  stop  the  blood  going  back  ;  there  would  be  a  murmur 
then.  And  when?  Why,  after  the  first  sound  of  the 
heart  has  gone  by,  after  the  contraction  of  the  ventricle — 
in  the  period  of  rest,  or  in  the  place  of  the  second  sound. 
A  murmur,  then,  heard  at  the  base  of  the  heart  in  the 
place  of  the  second  sound,  implies  regurgitation ;  a  mur- 
mur heard  during  the  contraction  of  the  heart  implies  ob- 
struction. You  may  have  both  in  the  same  person,  at  the 
same  time.  Again,  if  there  is  vegetation,  if  there  is  un- 
natural thickening  of  the  mitral  valve,  when  the  blood 
passes  from  the  auricle  into  the  ventricle  during  the  period 
of  repose,  there  may  be  a  murmur.     It  is  almost  always  a 


12  HEART  SOUNDS. 

very  faint  murmur,  and  Dr.  Williams  described  it,  a  good 
many  years  ago,  as  being  like  the  sound  produced  by 
breathing  the  word  awe — a  very  soft  blowing  murmur. 
That  is  in  the  period  of  rest ;  it  has  been  called  presysto- 
lic. I  have  no  objection  to  the  name ;  it  is  before  the 
systole. 

Dr.  Flint  {Am.  Jour.  Med.  Set.,  April,  1882,)  recognizes 
two  very  distinct  tones  in  the  presytolic  murmur :  one  soft 
blowing,  compared  by  Williams,  senior,  to  sound  produced 
by  the  breathed  word  awe;  the  other  rough,  resembling  the 
sound  produced  by  blowing  over  a  piece  of  paper,  one  end 
of  which  is  attached  to  the  lower  lip.  He  recognizes  with 
others  the  fact  that  the  soft  sound  is  but  rarely  heard, 
while  the  rough  sound  is  not  very  uncommon.  He  thinks 
it  is  produced  by  vibrations  of  the  curtain  of  the  mitral 
valve  caused  by  the  passage  of  blood  from  the  auricle  into 
the  ventricle.  "A  rough  presystolic  murmur,"  he  says, 
"  exceptionally  is  produced  when  there  is  no  mitral  lesion, 
aortic  regurgitation  existing  whenever  the  murmur  is  thus 
produced."  He  says  that  Fauvel  recognized  the  rough 
murmur  in  1843,  ^^^  called  it  bruit  de  rape,  and  established 
its  connection  with  the  mitral  obstructive  lesion. 

Then  you  may  have  two  murmurs  at  each  one  of  these 
valvular  openings ;  in  which  case  it  is  obstruction  in  the 
one  instance  and  regurgitation  in  the  other.  Now,  to 
satisfy  yourself  whether  it  is  obstructive  or  regurgitative, 
you  have  only  to  remember  the  course  of  the  blood.  From 
the  auricle  it  passes  into  the  ventricle  during  the  period  of 
rest ;  then  the  ventricle  contracts  and  it  passes  over  these 
valves  into  the  aorta,  or  if  the  valves  are  diseased  the 
blood  is  regurgitated. 

Then,  too,  it  sometimes  happens,  as  I  shall  explain  to 
you  further  on,  that  these  valves  are  subjected  to  a  cer- 
tain amount  of  inflammatory  action  when  endocarditis 
occurs,  and  their  action  is  disordered.     The  mitral  valve, 


HEART   SOUNDS.  1 3 

we  know,  is  composed  of  fleshy  columns,  which  are  com- 
posed of  fibres  that  are  continuous  with  those  in  the  walls 
of  the  heart.  Now,  if  these  be  diseased,  one  or  more  of 
them,  or  a  part  of  one  may  become  contracted  and 
leave  an  opening  in  the  mitral  valve.  This  fact  shows 
that  regurgitation  may  take  place  without  disease  of  the 
valves,  that  is,  without  deforming  disease  of  the  valves. 

As  the  blood  comes  from  the  ventricles  it  is  forced  over 
the  semilunar  valves,  which  lie  smoothly  up  against  the 
aorta,  presenting  no  obstruction  to  the  outgo  of  the  blood. 
If  they  are  rough,  thickened,  contracted,  then  they  will 
present  an  obstacle  to  the  course  of  the  blood,  and  there 
will  be  produced  a  murmur  during  the  contraction  of  the 
heart,  that  is,  during  systole — the  time  when  you  feel  the 
impulse  of  the  heart  against  the  ear  when  it  is  applied  to 
the  chest.  Now,  that  is  easily  remembered,  I  think  ;  the 
murmur  in  systole,  the  murmur  in  the  contraction  of  the 
ventricle,  heard  over  that  part  of  the  chest  which  corre- 
sponds to  the  aorta,  an  aortic  obstruction.  When  the 
blood  reaches  the  aorta,  the  aorta  dilates,  and  on  account 
of  the  many  little  elastic  fibres  which  it  contains  it  has  a 
disposition  at  once  to  contract ;  and  in  contracting  it  of 
course  starts  the  current  backward  toward  the  heart, 
which  instantly  closes  these  valves  and  thus  prevents  its 
return.  But  if  these  valves  have  become  so  thickened, 
so  hard  and  inelastic  that  they  will  not  close,  a  portion  of 
the  blood  is  sent  back  into  the  ventricle,  which  has  to 
do  its  work  over.  This  produces  a  murmur  which  occurs 
during  the  period  of  repose  or  in  the  place  of  the  second 
sound.  This  constitutes  aortic  regurgitation.  We  often 
have  obstruction  and  regurgitation  in  the  same  person,  so 
that  we  will  have  a  "  whewing"  sound  during  contraction, 
which  is  repeated  during  diastole  of  the  ventricle.  It  has 
come  to  be  the  fashion  of  late  to  use  the  terms  "  direct" 
and  "  indirect."     I  do  not  think  the  terms  nearly  as  good 


14  HEART  SOUNDS. 

as  obstruction  and  regurgitation,  for  these  are  descriptive, 
while  only  "  direct"  can  be  regarded  as  descriptive  in  the 
other  choice  of  terms. 

Then  the  blood  passes  on  in  the  general  circulation,  and 
comes  back  in  the  veins  to  the  other  side  of  the  heart,  to 
the  right  auricle.  The  right  auricle  in  turn  contracts  after 
it  is  full,  and  sends  its  blood  into  the  right  ventricle, 
which,  being  connected  with  the  left  ventricle  by  the 
septum,  is  really  a  part  of  the  same  organ,  and  liable  to 
contract  at  the  same  time  ;  and  the  right  and  left  ventri- 
cles then  do  contract  at  the  same  instant,  and  a  sound 
produced  by  the  passage  of  blood  into  the  pulmonary 
artery  occurs  in  systole.  You  observe  that  the  pul- 
monary artery  has  valves  corresponding  with  those  of 
the  aorta,  and  they  work  in  the  same  way.  They  fall  up 
against  the  artery,  and  allow  the  blood  to  flow  over  them 
easily  and  freely.  But  these,  too,  are  sometimes  found 
to  be  diseased.  The  valves  of  the  right  side  of  the  heart, 
I  say,  are  sometimes  found  to  be  diseased,  and  here  is  as 
good  a  place  to  state  the  fact  as  any,  that  in  persons  who 
have  disease  of  the  right  side,  if  it  is  not  due  to  laceration 
or  breaking  of  the  tendinous  cords,  you  may  pretty  rea- 
sonably infer  that  the  disease  belonged  to  the  period 
before  birth.  The  right  side  of  the  heart  is  more  subject 
than  the  left  to  disease  in  utero.  The  left  side  of  the 
heart  becomes  diseased  after  birth.  If  you  can  find  a 
murmur,  then,  that  belongs  to  the  pulmonary  valves,  you 
will  be  pretty  sure  to  find  it  in  a  child,  and  it  will  be 
pretty  safe  to  infer  that  there  was  endocarditis  in  that 
child  before  it  was  born.  It  is  not  a  common  occurrence, 
and  yet  it  has  happened  a  few  times  in  my  experience. 
Then  the  same  law  applies  to  the  current  of  blood  and 
to  the  sound  that  will  be  produced  by  disease  of  the 
valves  of  the  right  side  as  on  the  left.  There  are  two 
valves  here,  the  tricuspid,  which  guard   the  opening  be- 


HEART  SOUNDS.  1 5 

tween  the  auricle  and  ventricle,  and  act  in  the  same  way 
as  the  mitral  valve  on  the  left  side,  and  the  pulmonary- 
valve. 

Now,  I  will  repeat  the  formula  by  which  you  can  recog- 
nize disease  at  different  points  of  the  heart.  Remember 
that  these  fleshy  columns  are  connected  with  the  heart  at 
a  distance  of  from  one  inch  to  an  inch  and  a  half  above 
its  apex  ;  these  tendinous  cords  run  into  the  heart,  and 
may  be  regarded  as  conducting  media,  and  the  fleshy 
columns  also  may  be  regarded  as  conducting  media. 
The  point  where,  physiologically,  in  audition,  you  can  get 
nearest  to  the  heart,  is  not  at  the  apex  exactly,  but  about 
an  inch  above.  There  you  will  be  more  likely  to  hear 
sounds  produced  in  the  mitral  valve  than  at  any  other 
part  of  the  chest ;  and  when  I  say  "  heard  at  the  apex," 
I  mean  at  the  apex,  or  an  inch  above.  When,  then,  you 
have  a  murmur  during  the  time  the  ventricle  is  being 
filled,  you  ascertain,  by  listening  at  different  points,  where 
it  is  most  distinct.  If  it  is  most  distinct  at  or  near  the 
apex  in  systole,  it  is  a  murmur  of  regurgitation  at  the 
mitral  valve  ;  if,  on  the  contrary,  it  is  heard  in  the  period 
of  repose,  the  blood  is  flowing  from  the  auricle  into  the 
ventricle,  and  that  will  be  an  obstructive  sound  in  the 
mitral.  The  mitral  is  roughened,  and  throws  the  blood 
or  itself  into  sonorous  vibrations,  as  the  blood  flows  over 
it ;  that,  however,  is  almost  always  a  very  feeble  sound. 
As  I  said  before.  Dr.  Williams  described  it  by  breathing 
the  word  "  awe,''  opening  the  throat  well  and  breathing 
a  little  loud. 

A  murmur  heard  most  distinctly  on  the  third  rib,  at 
the  sternum,  and  heard  in  systole,  must  be  obstruction  at 
the  aortic  valve.  Then,  if  it  is  repeated  immediately 
afterward,  in  the  interval,  you  can  hardly  appreciate  it, 
and  yet  you  do  appreciate  that  there  are  two  sounds — 
the  latter  is  regurgitation  ;  the  valve  acts  insufificiently. 


l6  HEART   SOUNDS. 

it  cannot  perform  its  office,  and  thus  the  murmurs  are 
produced.  Every  little  while  you  get  two  murmurs.  I 
have  heard  four  in  the  same  person,  two  produced  at 
the  aortic  valve,  two  at  the  mitral. 

Now,  the  same  law  applies  to  the  right  side  of  the  heart. 
You  listen  to  the  right  side  of  the  heart,  at  the  lower  part 
of  the  precordial  region  on  the  right  side.  I  do  not  say 
the  lower  part  of  the  sternum  extends  below  the  heart 
region ;  but  on  the  sternum  at  the  fifth  rib,  and  outside 
the  sternum  a  little,  on  the  same  level,  you  will  get  a 
sound  from  the  right  heart  more  distinctly  than  anywhere 
else.  If,  then,  you  get  a  murmur  in  that  region,  heard 
most  distinctly  in  contraction  of  the  heart,  in  systole,  that 
would  be  regurgitation,  at  the  tricuspid  valve.  If,  on  the 
contrary,  you  get  a  myrmur  which  you  are  not  quite  sat- 
isfied is  aortic,  and  it  is  a  little  to  the  left  of  the  sternum, 
you  may,  perhaps,  conjecture  tjjat  it  belongs  to  the 
pulmonary  artery.  The  pulmonary  artery  is  given  off  a 
little  further  to  the  left  than  the  aorta,  and  you  listen  for 
the  aortic  murmurs  on  the  middle  of  the  sternum  and  a 
little  to  the  right ;  for  the  pulmonary  murmurs  on  the  left 
edge  of  the  sternum  and  a  little  to  the  left  of  the  sternum. 
If  you  get  a  murmur  there  in  systole  it  is  due  to  obstruc- 
tion at  the  pulmonary  valve.  If  it  is  repeated,  it  is  then 
regurgitation  at  the  same  valve,  and  is  heard  most 
distinctly  at  the  base  of  the  heart.  But  if  it  is  a  tricuspid 
murmur  you  will  hear  it  most  distinctly  over  the  right  side 
of  the  heart,  at  the  right  edge  of  the  sternum ;  I  never 
have  heard  a  direct  or  obstructive  murmur  at  this  point. 
Indeed,  a  good  many  .years  ago  Dr.  King  thought  he 
demonstrated,  and  probably  he  did,  that  this  particular 
part  of  the  heart,  the  opening  of  the  tricuspid  valve,  has 
considerable  power  of  dilatation  without  injury,  and  when 
the  veins  are  overcrowded  with  blood,  surcharging  the 
left  ventricle,  he  claims  that  the  right  ventricle  has  the 


HEART  SOUNDS.  I7 

power  of  sending  it  back  into  the  veins  again  through  the 
tricuspid  opening  and  without  a  murmur.  I  can  easily 
comprehend  that  it  may  be  so.  It  is  what  he  called  the 
safety-valve  arrangement.  The  right  ventricle  being  over- 
distended  the  right  auriculo-ventricular  opening  would 
be  dilated  also,  and  a  part  of  the  blood  can  be  thrown 
back  into  the  veins  of  the  general  system  without  being 
compelled  to  go  forward  into  the  arteries  that  lead  to  the 
lungs. 

With  reference  to  the  tones  of  these  murmurs.  You 
hear  them  in  different  stages  of  cardiac  disease ;  mildly 
when  the  valves  begin  to  be  deteriorated ;  more  strongly 
when  the  deformity  has  become  considerable.  And  then 
again,  perhaps  not  at  all  after  the  disease  has  continued 
for  a  length  of  time,  and  the  heart  has  become  weakened 
by  it.  Almost  every  person  who  has  cardiac  disease  which 
finally  terminates  fatally  reaches  a  period,  before  death, 
when  the  murmur  cannot  be  heard,  and  the  simple  reason 
is  that  the  heart  cannot  contract  upon  its  contents  with 
sufficient  force  to  make  the  blood  run  swiftly  enough  to 
cause  a  murmur.  It  is  probable  that  these  murmurs  are 
made  in  the  solid  tissue  and  not  in  the  blood  itself.  The 
vibrations  that  produce  the  murmur  are  probably  in  these 
deformed  valves.  You  have  a  great  many  terms  by  which 
to  designate  these  murmurs,  according  to  their  tone.  The 
French  have  used  terms  which  represent  a  filing  sound,  a 
rasping  sound,  a  sawing  sound,  which,  of  course,  are  harsh, 
and  given  to  distinguish  the  harsh  sounds  from  those 
which  are  soft  and  blowing.  But  it  is  not  necessary  for 
you  to  learn  these  terms.  The  coarse  sounds  are  almost 
always  produced  by  deformity  or  defect  of  the  valves. 
The  blowing  sounds  are  often  produced  by  the  same 
thing,  but  they  are  also  produced  under  circumstances  in 
which  the  valves  are  not  diseased  ;  when,  for  example,  the 
blood  becomes  watery  and  thin,  by  a  law  which  I  cannot 


j8  HEART  SOUNDS. 

I  ^ 

explain  to  you,  the  blood  makes  a  noise  in  going  over  the 
aortic  valves.  It  is  the  anaemic  sound  ;  and,  therefore,  if 
you  hear  a,  blowing  sound  at  the  aortic  opening,  as  if  it 
were  obstructive,  your  next  business  is  to  look  in  the 
patient's  face  and  see  if  she  is  anaemic — for  anaemia  occurs 
more  frequently  in  women  than  in  men.  If  the  face  is 
pale  and  has  a  chlorotic  look,  you  will  be  very  likely  to 
get  a  soft  murmur— a  blowing  murmur  at  the  aortic  open- 
ing, and  it  will  not  authorize  you  to  infer  that  there  is  any 
disease  of  the  aortic  valves  under  such  circumstances. 

Dr.  G.  W.  Balfour*  has  lately  published  an  article  enti- 
tled "Arguments  in  Favor  of  the  Theory  of  Dilatation  of 
the  Heart  as  the  Cause  of  Cardiac  Haemic  Murmurs  and  of 
the  Appendix  Auriculi  Sinistri  being  the  Primary  Seat  of 
this  Murmur."  So  far  as  I  can  judge  from  the  analysis  of 
the  abstract  which  I  have  seen  (for  I  have  not  read  the 
whole  paper  as  published  in  the  Brit.  Med.  Jour.,  Aug.  26, 
1882),  it  is  arguments,  not  demonstration.  He  does  not 
even  adduce  convincing  proofs  from  auscultation.  The 
idea  has  met  with  criticism  already.  We  are  not,  then, 
converted  wholly  from  the  old  doctrine  that  the  haemic  or 
chlorotic  murmur  is  produced  at  the  valves  of  the  heart. 
That  in  the  same  state  of  the  system,  the  pressure  of  the 
stethescope  on  a  vein,  the  jugular,  for  example,  will  pror 
duce  a  continuous  murmur  {bruit  de  diable)  would  seem 
to  show  that,  in  chlorosis,  the  blood  changes  have  given 
to  that  fluid  the  capacity  of  producing  sound,  from  causes 
that  do  not  operate  in  that  way  in  health.  These  sounds 
are  often  called  anaemic,  but  immediately  after  a  large 
loss  of  blood  they  do  not  occur,  but  they  are  found,  if  at 
all,  after  the  vessels  are  replenished  by  absorption  of  fluid, 
and  its  constitution  thereby  greatly  changed.     This  has 


*  Medical  Record,  Nov.  i8,   1882,  p.  572,  whiqh  sep,  apd  N-  ¥•  Med, 
yi(7«n,  Dec,  1882,  p.  657. 


HEART  SOUNDS.  I9 

been  denominated  hydraemia,  and  the  name  is  not  an 
improper  one.  But  the  term  chlorosis  is  appHed  almost 
exclusively  to  a  condition  that  is  not  preceded  by  loss 
of  blood,  but  by  bad  assimilation,  and  ends  in  great 
reduction  of  the  nourishing  power  of  the  blood  ;  in  paleness 
and  a  puffy  condition  o.f  the  skin,  with  moderate  oedema 
and  loss  of  force.  This  is  the  disease  in  which  we  most 
frequently  hear  the  haemic  anaemic  sound. 

There  is  another  thing  connected  with  thin  blood  which 
may  perhaps  help  you  to  distinguish  the  sounds  that  are 
produced  by  deformity  of  the  valves  and  those  that  occur 
when  the  valves  are  sound.     Jan.   21,  1883,  a  boy  from 

M ,  8  years  of  age,  was  brought  to  me  by  his  parents. 

He  had  been  very  much  reduced  by  disease,  so  that  he  was 
very  pale  and  thin  and  had  aortic  systolic  murmurs,  and  his 
physician  found  serious  heart  disease.  From  his  anaemic 
state  he  had  rapidly  improved,  so  that  now  he  looked 
healthy  and  was  strong,  appetite  good,  almost  voracious, 
and  digestion  good.  Examining  him  to-day  there  is  no 
murmur,  the  heart  is  of  proper  size  for  a  boy  of  his  age. 
The  inference  is  conclusive  that  the  late  systolic  aortic 
murmur  was  a  blood  (haematic)  murmur,  which  his  im- 
proved health  has  removed.  In  most  of  these  persons  in 
whom  anaemic  murmurs  occur  there  will  be  heard,  through 
the  stethoscope  applied  over  the  jugular  vein  in  the  neck, 
a  continuous  humming  noise.  They  call  it  bruit  de  la 
toupie,  which  a  friend  of  mine  has  interpreted  with  a  little 
liberty,  ''devil  of  a  noise."  This  briiit  de  la  toiipie  is  not 
the  work  of  the  devil.  The  French  have  a  little  toy  which 
children  whirl  around,  and  as  it  goes  around,  a  spring 
works  on  a  wheel  of  cogs  and  makes  a  repetition  of  clicks. 
That  is  the  devil  that  this  is  compared  with — bruit  de  la 
toupie.  This  sound  is  not  connected  with  disease  of  the 
heart,  but  as  it  so  frequently  occurs  in  anaemic  persons  it 
is  worth  while  to  allude  to  it  in  this  connection.     The 


20      V  HEART  SOUNDS. 

harsh,  rasping  sound  is  almost  always  produced  by  sorae 
defect  of  the  valves ;  the  soft,  blowing  murmur  may  be  so 
produced,  but  it  is  occasionally  found  in  persons  whose 
hearts  are  sound  enough,  but  whose  blood  is  diseased  or  in 
a  watery  condition.  I  do  not  think  there  is  any  practical 
use  in  making  any  other  distinctions  between  the  soft 
and  the  harsh,  or  the  blowing  and  the  rough  murmur. 

Dr.  E.  Hyler  Graves*  concludes:  i.  The  presence  of 
murmurs  does  not  necessarily  indicate  the  existence  of 
incurable  lesions,  or  their  absence  that  such  lesions  are 
not  present ;  but  other  symptoms  must  be  looked  to  for  a 
correct  diagnosis.  2.  The  persystolic  murmur  of  mitral 
stenosis  may  disappear  and  the  lesion  remain.  Mitral 
regurgitant,  when  due  to  simple  relaxation  of  the  heart's 
muscles  and  dilatation  of  its  cavities  and  orifices,  as  in 
chlorosis  and  fever,  in  most  cases  completely  disappears. 
3.  Tricuspid  regurgitation  is  occasionally  temporary,  due 
to  bronchitis,  etc.  4.  Aortic  systolic  murmurs,  due  to 
permanent  lesion,  may  undergo  changes  in  intensity  but 
never  completely  disappear.  5.  Aortic  diastolic  murmurs 
in  rare  cases  have  been  known  to  disappear.  The  sys- 
tolic aortic  murmur  in  these  cases  is  always  present  and 
is  persistent.  6.  The  pulmonary  systolic  is  permanent 
when  due  to  organic  lesion,  but  is  non-organic ;  may  dis- 
appear temporarily  or  permanently. 

There  is  another  thing  that  I  must  call  your  attention 
to  before  discussing  endocarditis  itself. 

At  the  83rd  meeting  of  the  Medical  and  Chirurgical 
Faculty  of  Maryland,  April,  i88i,t  Dr.  John  S.  Lynch 
communicated  a  new  plan  in  the  differential  diagnosis  of 
cardiac  and  pericardial  murmurs.  He  said,  ^'  Whenever 
the  friction  murmur  is  produced  at  or  near  the  apex  of  the 


*  Med.  Rec,  Sep.  29,  1883. 

\  Am.  Jour,  of  Med,  Sci.j  Oct.,  1882, 


tiEART  SOUNDS.  it 

heart,  if  we  cause  the  patient  gradually  and  slowly,  but  en- 
tirely to  inflate  the  lungs,  we  will  perceive  that  the  friction 
murmur  becomes  gradually  progressively  more  intense 
until  the  act  of  insufflation  is  complete.  Now  make  the 
patient  *  hold  his  breath '  while  the  lungs  are  in  this  state, 
and  the  murmur  will  be  steadily  maintained  at  its  maxi- 
mum intensity;  cause  him  then  to  expire  in  a  like  slow 
and  gradual  manner,"  and  the  reverse  will  be  observed. 
He  thinks  the  sound  at  the  apex  is  the  only  one  that 
presents  any  difficulty  in  diagnosis. 

The  heart  itself  has  two  sounds.  They  are  denominated 
first  and  second,  and  it  will  interest  you  to  know  what  is 
the  cause  of  these  two  sounds  ;  and,  perhaps,  as  great  di- 
versity of  opinion  has  been  expressed  in  regard  to  this,  it 
may  be  of  some  little  interest  to  you  to  know  which  opin- 
ion I  have  chosen. 

As  a  consequence  of  the  arrangement  of  the  muscular 
fibres  of  the  heart,  as  the  heart  contracts,  all  these  bun- 
dles of  fibres  contract  at  the  same  time,  and  one  rubs 
against  another.  It  is  not  exactly  a  fiddle-string  opera- 
tion, and  yet  it  is  not  without  analogy  to  it.  These 
fibres  cannot  rub  upon  one  another  actively,  as  they  do 
when  the  heart  contracts,  without  producing  some  sound, 
and  this  first  sound  continues  during  the  contraction  of 
the  heart.  It  begins  with  the  beginning  and  ends  with 
the  end  of  that  contraction — that  is,  of  the  ventricles.  The 
auricles  are  placed  a  little  out  of  hearing,  so  that  you  can- 
not know  what  is  going  on  in  them  by  audition.  You 
can  imitate  the  sound  very  closely  by  placing  the  stetho- 
scope upon  the  ball  of  the  thumb  and  opening  the  thumb. 
You  will  hear  a  sound  exactly  like  that  which  is  produced 
by  the  first  sound  of  the  heart.  Another  very  good  illus- 
tration of  this  sound  may  be  had  by  placing  the  arm 
against  something  that  is  firm  and  extending  and  con- 
tracting  it,  and  listening  to  the  action  of  the  muscles. 


±2  HEART  SOUNDS. 

It  has  been  said  that  the  first  sound  is  produced  by  the 
tension  of  the  mitral  valves,  in  consequence  of  the  sudden 
jerk  made  upon  them  by  their  muscular  columns.  I  do 
not  know  that  that  does  not  enter  into  the  first  sound 
and  make  a  part  of  it ;  I  do  not  know  that  it  does.  It 
has  been  said,  again,  that  the  first  sound  is  produced  by 
the  rush  of  blood  from  the  auricle  into  the  ventricle  (?). 
I  do  not  know  but  that  this  aids  in  the  pro'duction  of  the 
first  sound,  and  I  do  not  know  that  it  does.  The  current 
is  easy,  the  flow  is  at  a  pretty  good  rate,  to  be  sure,  and 
I  should  not  be  surprised  if  concussion  against  the  empty 
walls  of  the  ventricles  would  produce  some  effect  of  that 
kind  ;  and  yet  I  do  not  know  it. 

I  think  when  you  have  tried  these  little  experiments  I 
have  spoken  to  you  of,  and  then  listen  to  the  heart  sounds 
you  will  be  pretty  well  satisfied  that  the  chief  element  in 
it  is  the  contraction  of  the  muscles,  and  the  rubbing  of 
these  cross-fibres  one  against  another.  They  are  sepa- 
rated, to  be  sure,  by  a  little  layer  of  connective  tissue, 
but  even  that  is  put  upon  the  stretch  by  the  action  of 
these  muscles  that  are  working  at  right-angular  contrac- 
tion. The  first  sound,  therefore,  is  confined  entirely  to 
the  systole,  to  the  contraction.  The  second  sound  there 
are  no  debates  about ;  experiments  have  been  performed 
that  explain  that  perfectly.  A  number  of  physicians  in 
London  tortured  some  honest  old  asses  and  worn-out 
horses,  by  opening  the  chest  and  having  little  hooks  that 
were  sharp  enough  to  penetrate  the  tissue,  laying  the  hook- 
handle  along  the  course  of  the  aorta  and  penetrating  it, 
then  carrying  the  hook  forward  and  getting  it  over  one  of 
the  folds  of  the  semilunar  valve,  and  drawing  it  back  up 
to  the  wall  of  the  artery.  It  is  an  experiment  that  can 
be  pretty  easily  done.  The  result  of  the  experiment  was 
a  cessation  of  the  second  sound.  Then  by  depressing  the 
handle  and  raising  the  point  of  this  hook  the  valve  would 


Heart  sounds.  .        ^5 

be  let  loose,  and  be  at  liberty  to  play  again,  and  then  the 
second  sound  was  reproduced.  They  repeated  the  ex- 
periment a  great  many  times,  and  in  a  great  variety  of 
ways.  A  Philadelphia  committee  of  doctors  repeated  it 
with  the  same  result,  so  that  we  have  the  fact  pretty  well 
established,  that  the  second  sound,  which  you  will  recog- 
nize as  instantaneous  as  a  click,  results  from  the  falling 
together  of  these  three  segments  of  the  valve  in  the  cen- 
tre of  the  aorta. 

When  the  second  sound  of  the  heart  is  unusually  loud,  it 
has  been  the  habit  of  late  to  say  that  it  is  accentuated.  This 
word  may  not  be  the  best  that  could  have  been  chosen, 
but  it  appears  to  have  the  sanction  of  usage,  and  that 
entitles  it  to  the  place  it  occupies.  This  intensified  second 
sound  may  be  noticed  on  either  side  of  the  heart,  that  is, 
it  may  be  seated  either  in  the  pulmonary  or  in  the  aortic 
valve.  In  either,  two  conditions  of  the  organ  are  neces- 
sary. It  must  retain  a  good  deal  of  its  natural  strength, 
and  the  valves  referred  to  must  be  sound,  or  if  not  entirely 
free  from  disease,  not  diseased  in  a  way  to  impair  their 
efficiency.  Another  condition  is  equally  necessary — that 
the  flow  of  blood  from  the  half  of  the  heart  in  which  it  is 
produced  be  resisted.  The  familiar  second  sound  in  the 
pulmonary  artery,  when  there  is  stenosis  of  the  mitral  is  an 
example.  Any  obstruction  in  the  pulmonary  circulation, 
the  heart  retaining  its  strength,  the  valve  its  integrity,  and 
the  quantity  of  blood  in  the  system  undiminished,  will  pro- 
duce it  in  the  same  way.  Pneumonia  produces  it  unless 
the  heart  is  feeble.  Phthisis  does  not,  because  the  vol- 
ume of  blood  in  the  body  is  diminished,  as  is  also  the 
strength  of  the  heart. 

Dr.  Begbie  has  found  that  sacculated  aneurism  and 
dilatation,  or  true  aneurism  of  the  aorta,  produce,  with  a 
good  deal  of  constancy,  exaggerated  second  sound  at  the 
aortic  opening.     The  probable  explanation  of  this  is  that 


24  HEART  SOUNDS. 

as  neither  of  these  changes  occurs  spontaneously  without 
atheromatous  deposit  in  the  vessel,  that  while  the 
strength  of  its  walls  is  diminished,  their  distensibility  is 
also  decreased. 

You  would  naturally  expect,  if  these  aortic  valves  were 
inefficient,  and  did  not  guard  the  opening,  that  there 
would  be  no  second  sound  produced.  But  call  to  mind 
the  fact  that  I  just  now  stated  to  you  that  the  two  hearts 
beat  at  the  same  time,  and  it  is  almost  never  found  to  be 
the  case  that  the  pulmonary  valves  and  the  aortic  valves 
are  diseased  in  the  same  person.  You  have,  then,  the 
pulmonary  valves  to  give  you  the  second  sound.  The 
aortic  valves  may  not  participate  in  it,  may  not  fall  to- 
gether at  all ;  they  may  be  too  short  and  too  inflexible. 
The  cause,  then,  of  the  two  sounds  of  the  heart  you  can 
easily  carry  in  mind.  The  reflux  of  the  blood  from  the 
aorta  in  its  attempt  to  get  back  into  the  ventricles,  closes, 
as  I  told  you,  these  valves;  they  close  with  a  click,  and 
that  is  all  there  is  of  the  second  sound. 

The  sphygmograph  is  now  pretty  well  known,  and  its 
indications  pretty  well  understood.  It  will  indicate  aor- 
tic obstruction  by  the  sloping  rise  of  its  tracing ;  aortic 
regurgitation  by  the  rapid  fall ;  irregular  action  of  the 
heart  by  its  writing  down  the  small  and  varying  action 
with  more  correctness  than  the  finger  on  the  artery  can 
possibly  attain ;  and  yet  its  diagnostic  value  is  not  great, 
for  almost  all  that  it  teaches  that  is  important  can  be 
learned  by  other  and  shorter  methods. 

But  now  there  is  a  compound  sphygmograph,  by  which 
the  beating  of  the  pulse  of  any  artery,  and  the  beating  of 
the  heart  are  recorded  on  the  same  paper,  one  tracing 
over  the  other  with  a  time  index  at  the  bottom.  It 
shows  how  much  the  pulse  wave  in  any  artery  chosen  for 
the  experiment  is  delayed,  after  the  heart  has  contracted, 
or  on  the  other  hand,  if  the  pulse  wave  reaches  the  artery 


HEART   SOUNDS.  25 

under  examination  in  less  time  than  the  normal,  how 
much  it  is  accelerated.  As  each  contraction  of  the  heart 
and  the  pulse  produced  by  it  is  traced  one  above  the 
other,  it  is  easy  to  compare  them,  and  to  learn  the  time 
difference  between  them.  But  that  this  difference  may 
be  useful,  the  natural  or  normal  difference  between  the 
heart  beat  and  the  pulse  beat  in  the  several  arteries  must 
be  known.  This  basis  fact  is  apparently  ascertained. 
Dr.  A.  T.  Keyt  announces  that  the  time  consumed  by 
the  pulse  wave  in  passing  to  the  carotid  artery  is  -^  of  a 
second ;  to  the  temporal  in  front  of  the  auditory  meatus, 
■^  o{  2i  second  ;  to  the  radial,  ^ ;  to  the  femoral,  -I-;  to  the 
artery  on  the  upper  surface  of  the  foot,  ^.  These  are 
averages.  If  they  are  confirmed  they  make  an  interesting 
demonstration  of  the  rate  at  which  the  blood  travels  in 
the  vessels.  It  is»  claimed  that  dilatable  aneurism,  stiff 
aortic  valves  and  mitral  regurgitation  delay  the  wave,  and 
make  the  time  longer;  while  aortic  regurgitation  and 
rigid  arteries  make  it  shorter.  Dr.  A.  B.  Isham  of  Cin- 
cinnati has  pubhshed  a  paper  on  the  application  of  this 
instrument  to  diagnosis  {Am.  Journ,  of  Med.  Science^ 
July,  1882,)  in  which  he  gives  a  considerable  number  of 
cardiac  and  arterial  tracings,  one  over  the  other.  The 
greatest  difference  that  he  has  recorded  is  ||-  of  a  second 
between  the  heart  and  the  right  subclavian,  while  in 
health  the  time  should  be  -f^.  This  is  certainly  a  marked  re- 
tardation— one  that  could  be  recognized  but  not  measured 
without  the  aid  of  the  instrument.  It  occurred  in  a  per- 
son who  had  aneurism  of  the  aorta  and  mitral  regurgita- 
tion. In  a  case  of  mitral  regurgitation  the  pulse  in  the 
carotid  (right?)  was  delayed  \  to  \y  instead  of  ^  of  a 
second.  But  these  are  large  delays.  In  a  case  in  which 
the  aortic  opening  was  greatly  obstructed,  the  delay  in 
the  carotid  (right?)  was  J  of  a  second,  while  the  natural 
delay  is-^oidi  second.     This  case  is  narrated  by  Dr.  A.  T« 


^6  ittEARt  SOUNDS. 

Keyt,  in  the  Cincinnati  Clinic,  April  19,  1879,  ^^^  ^^  the 
Medical  Record,  June  4,  1881.  I  have  been  sufficiently 
interested  in  the  use  of  this  instrument  to  try  to  obtain  one, 
but  it  must  be  imported,  and  my  confidence  in  its  prac- 
tical value  has  not  yet  overcome  this  trifling  obstacle  ;  for 
so  far  its  teachings  are  more  confirmatory  of  what  can  be 
learned  by  other  means,  than  an  instrument  communicat- 
ing new  information.  But  as  the  shrub  may  grow  into  a 
tree,  the  moderate  beginning  of  the  cardiac  sphygmo- 
graph  may  have  a  large  and  expanded  growth. 

Heart  Scanning. — Dr.  Samuel  W.  Francis  says  that  the 
normal  beat  of  the  healthy  heart   is  iambic  ^^  — ;    that 

when  it  is  trochaic  —  ^^,  pyrrhic  -^  -~-  or  spondaic , 

these  measures  indicate  disease.  He  also  reports  a  case 
in  which  the  pulse  was  only  29  in  the  minute,  and  the 
beat  dactylic  —  ^  ^-^,  a  long  and  two  short  being  well 
marked.  The  patient  was  a  lady  sixty  years  of  age,  who 
recovered  under  diffusive  stimulants,  and  counter-irrita- 
tion.    {The  Medical  Record,  Feb.  24,  1883.) 

Dr.  Henry  Cook  has  quoted  three  cases  published  by 
Dr.  Hyde  Salter,  and  added  three  of  his  own,  in  which 
the  rhythm  of  the  heart  was  lost  in  a  double  beat,  one 
following  the  other  so  quickly,  that  there  was  hardly  time 
enough  between  them  to  perceive  that  there  were  two — 
the  end  of  one  instantly  followed  by  the  beginning  of  the 
other.  The  second  systole  was  followed  by  a  second 
sound,  but  the  first  was  not.     Thus, 


instead  of 


In  these  cases  the  first  of  the  double  beat  sent  a  pulse  to 
the  wrist,  the  other  did  not;  but  in  one  of  Dr.  Salter's 
cases  this  was  changed.  At  the  first  examination  it  was 
the  first  of  the  two  beats  that  produced  the  radial  pulse ; 


HEART  SOUNDS.  2^ 

at  another,  he  says  "  the  second  beat  of  each  couple  was 
the  strongest,  not  the  first  as  formerly,  and  the  only 
one  reaching  the  wrist,  though  the  first  and  feebler  was 
plainly  visible  in  the  carotids." 

In  four  of  these  six  cases  it  was  noticed  that  the  time 
occupied  by  this  double  beat  and  the  pause  following,  was 
just  double  that  required  for  a  single  beat  and  pause.  For 
example,  if,  while  the  heart  had  a  single  beat  and  pause, 
the  pulses  were  io6,  when  the  double  beats  occurred  it 
would  be  53.  Both  observers  had  the  opportunity  of 
listening  to  the  heart  at  the  moment  the  change  from 
double  to  single  beat  occurred,  and  Dr.  Cook  witnessed 
the  change  from  single  to  double.  The  change  in  each 
direction  was  not  attended  with  the  slightest  disturbance ; 
indeed  of  one  patient  it  is  said  he  did  not  know  that  any 
change  had  occurred. 

In  a  man  who  had  aortic  obstruction,  and  both  tricuspid 
and  mitral  regurgitation,  Dr.  Cook  says,  "  each  impulse 
was  accompanied  with  the  systolic  bruit."  He  does  say 
that  there  was  disease  of  the  pulmonary  valve,  and  no 
post-mortem  examination  is  reported. 

These  double  beats  were  strong,  each  a  good  deal 
stronger  than  the  single  beat,  though  not  always  of  equal 
strength.  Neither  of  these  gentlemen  entertained  any 
doubt  that  it  was  a  double  action  of  the  left  ventricle, 
and  Dr.  Cook  devotes  considerable  space  to  conjectural 
explanations  of  the  mode  in  which  it  was  effected,  none 
of  which  seem  to  himself  wholly  satisfactory.  Was  it  not 
that  the  beat  of  the  right  heart  followed  that  of  the  left 
when  the  radial  pulse  was  produced  by  the  first  contrac- 
tion, and  opposite  when  the  pulse  attended  the  second? 
But  can  the  action  of  the  two  hearts  be  partly  separated 
in  that  way?  Some  recent  experiments  referred  to  else- 
where seem  to  prove  that  it  can  be,  in  animals,  and  to  a 


28  HEART  SOUNDS. 

much  greater  extent  than  is  necessary  to  explain  Drg. 
Salter  and  Cook's  cases.  But  I  have  myself,  not  fre- 
quently, to  be  sure,  but  two  or  three  times  recognized  a 
double  second  sound,  one  following  the  other  quickly, 
but  each  perfectly  distinct,  and  have  called  the  attention 
of  persons  who  were  with  me  to  the  fact  as  showing  a 
lack  of  strict  coincidence  in  the  action  of  the  two  hearts. 
Dr.  Cook  has  given  sphygmographic  tracings  of  his  cases, 
which  appear  to  be  conclusive  on  this  point.  If  the  two 
beats  were  both  left  ventricle  contractions,  when  the  trac- 
ings reached  the  highest  points,  they  must  be  held  there 
during  all  the  time  of  the  second  beat  of  the  couple,  with 
perhaps  a  downward  notch  between  the  two.  But  there 
is  nothing  of  the  sort.  The  descending  line  pays  no  at- 
tention to  the  second  beat,  but  descends  at  the  acutest  of 
angles,  greatly  more  acute  than  when  the  tracing  is  of  the 
normal  and  regular  beats. 

The  only  facts  that  seem  inconsistent  with  this  expla- 
nation are,  first,  the  statement  that  Dr.  Salter  noticed  a 
pulse  in  the  carotids  when  it  did  not  reach  the  radial 
artery.  But  may  not  a  full  wave  in  the  heart  give  a  pulse 
to  the  aorta  and  pulmonary  artery  that  would  extend  to 
the  carotids  ?  The  two  ventricles  so  commonly  contract 
at  the  same  instant  that  observations  are  yet  to  be  made 
which  will  enable  us  to  answer  this  question  positively. 
But  the  affirmative  answer  seems  to  me  probable.  Second,. 
Dr.  Cook  says  that  in  the  case  in  which  all  the  valves  were 
diseased  except  the  pulmonary  *'  There  were  now  two 
impulse  beats,  then  a  second  sound,  and  then  a  long 
pause,  and  each  impulse  was  accompanied  with  a  systolic 
bruit."  If  this  statement  is  strictly  correct,  there  must 
have  been  disease  of  the  pulmonary  valve  also.  At  least 
it  is  easier  to  suppose  this  than  to  admit  that  a  ventricle 
just  emptied  of  blood  could  empty  itself  again  on  the  in- 
stant, without    time  to  get   a   new  supply,  and  further, 


HEART  SOUNDS.  29 

with  no  power  to  make  a  pulse. — New  York  Medical  Ab- 
stract,  Feb.,  1882. 

Cardiac  Irregularities. — Dr.  Lukjanow,  not  long  ago, 
tried  the  effect  of  closing  one,  and  then  the  other  of  the 
coronary  arteries  of  the  heart ;  and  asphyxia  on  rabbits 
and  dogs.  The  function^-l  connection  of  the  different  parts 
of  the  heart  was  interrupted  by  the  closure  of  one  coron- 
ary artery.  A  difference  in  the  number  of  contractions  of 
the  auricles  and  ventricles  was  easily  produced,  and  almost 
as  easily  a  difference  between  the  two  auricles.  ''  Asyn- 
chronism  is  produced  in  the  auricles  much  more  readily 
than  in  the  ventricles."  The  closure  of  one  coronary  is 
found  to  influence,  first,  the  ventricle  on  the  same  side ; 
then  the  other  ventricle,  and  lastly  the  auricles."  The  car- 
diac muscle  may  contract,  he  says,  in  paristalsis,  or  in 
anti-peristalsis.  Sudden  asphyxia  especially  effects  some- 
times one,  sometimes  the  other  side  of  the  heart.  He 
attributes  these  phenomena  to  ''  the  effect  of  sudden 
ischaemia,  and  to  the  retention  in  the  tissues  of  the 
products  of  such  action  as  may  occur." — Am.  Jour,  of 
Med.  Sci.,  Apr.,  1882. 

If  these  experiments  can  be  relied  on,  asynchronism 
can  be  produced  by  local  anaemia  and  by  asphyxia,  and  if 
by  these  causes  in  all  probability  by  others  not  yet  under- 
stood. There  is  no  chance  closure  of  either  coronary 
artery  in  either  of  these  patients,  but  the  circulation  may 
have  been  modified  by  atheromatous  or  calcareous  de- 
posits in  one  of  them,  or,  as  is  most  probable  the  asyn- 
chronism came  from  some  unexplained  condition  of  the 
nerves  of  the  heart. 

As  to  these  heart  nerves  Dr.  E.  P.  Hurd  {The  Medical 
Record,  Oct.  28,  1883,)  writing  of  the  Physiology  of  the 
Jleart,  says  the  cardiac  innervation  comprehends  certain 
intra-cardiac  ganglia,  extra-cardiac  ganglia  and  nerves 
derived  from  the  sympathetic  and  cerebro-spinal  system. 


30  HEART  SOUNDS. 

Intra-cardiac  Ganglia. — These  are  in  the  walls  of  the 
heart,  and  regulate  the  rhythmical  working  of  the  cardiac 
muscle.  This  is  a  property  of  the  myocardium  itself 
also.  The  ganglia  of  Remak  are  placed  at  the  point 
where  the  sympathetic  and  pneumogastric  nerves  enter 
the  heart,  whose  terminal  filaments  are  lost  in  these 
ganglia.  They  occupy  thesinus  of  the  vena  cava.  Other 
gangHa,  those  of  Bidder  and  Ludwig,  are  situated  in  the 
auriculo-ventricular  furrow.  In  these  ganglia  originate 
fibres,  some  of  which,  centrifugal,  are  distributed  to  the 
muscular  fasciculi,  others,  centripetal,  terminate  in  the 
endo-cardium.  These  ganglia  and  these  nerves  constitute 
the  excito-motor  arc,  and  are  to  a  certain  extent  inde- 
pendent nerve  centres. 

Extra-cardiac  Gajiglia. — Almost  every  nerve  centre  has 
some  connection  with  the  heart,  but  the  cardiac  centre 
emphatically  is  in  the  rachidian  bulb  between  the  tuber- 
cula  quadragemina  and  the  thalamus.  When  this  is 
stimulated  by  a  strong  electrical  current  the  heart's 
action  is  arrested  or  slowed  by  a  less  powerful  current. 
If  previously  the  pneumogastric  nerves  are  cut  excitation 
here  produces  cardiac  acceleration.  The  medulla  ob- 
longata is  especially  the  centre  of  impressions  which 
reflexly  affect  the  frequency  and  rhythm  of  the  cardiac 
movements. 

Other  extra-cardiac  ganglia  exist  in  the  cervical  portion 
of  the  spinal  cord.  These  maybe  regarded  as  the  centres 
of  the  accelerator  nerves.  Von  Bezold  has  shown  that 
excitation  of  the  spinal  cord,  especially  in  its  upper  por- 
tion, augments  the  energy  of  the  heart  and  the  arterial 
pressure.  These  auxiliary  cardiac  ganglia  are  in  the 
closest  relation  with  the  vaso  motor  centre,  and  any  ex- 
citation which  raises  the  arterial  tension  may  be  attended 
by  accelerated  cardiac  action.  Ludwig  and  Thery  have 
clearly  proved  this  intimate  relation. 


.^  HEART  SOUNDS.  3! 

The  depressor  nerve  of  Cyon  is  a  sensory  nerve  found 
among  the  filaments  of  the  pneumogastric,  coming  with 
it  from  the  medulla  oblongata.  An  excitation  of  its 
terminal  branches,  endo-cardial,  is  reflected  on  the 
splanchnic  nerves  opens  the  splanchnic  vessels,  so  that 
the  heart  work  is  lessened  and  the  blood  pressure 
lower. 

The  vaso-motor  nerves,  when  they  contract  the  vessels, 
make  more  work  for  the  heart  and  increase  its  beatings. 
This  effect  is  witnessed  when  the  splanchnic  nerve  is  ex- 
cited by  electricity,  the  blood  pressure  is  increased  and 
the  heart  beats  are  quickened,  and  contrarywise. 

There  are  a  few  points  in  reference  to  the  anatomy  of 
the  heart  which  are  necessary  to  the  clear  understanding 
of  the  diseases  of  the  organ,  and  these  we  shall  proceed 
to  touch  upon. 

Other  investigators  report  observations  on  the  blood 
pressure  in  the  coronary  artery  and  the  carotid.  Simul- 
taneous tracings  taken  in  a  branch  of  the  left  coronary 
artery,  and  in  a  carotid  agree  in  every  respect.  If  the 
aortic  valve  closes  the  coronaries  during  systole,  the 
period  of  greatest  pressure  in  the  arteries  of  the  heart 
should  follow  the  same  period  in  the  carotid.  When 
one  inspects  the  aortic  valves  (N.  V.  Med.  Jour.,  March 
3,  1883,)  lays  them  up  against  the  aorta,  and  sees  how 
completely  they  cover  the  openings  of  the  coronary 
arteries,  and  must  cover  them  when  the  valve  is  open, 
it  is  much  easier  to  believe  that  these  gentlemen  have 
made  some  mistake  in  their  experiment,  or  in  their  ex- 
planation of  it,  than  to  abandon  the  apparently  inevitable 
inference  from  this  piece  of  anatomy.  But  if  the  experi- 
ment is  correctly  reported,  does  it  prove  any  more  than 
that  the  blood  pressure  is  greatest  in  the  coronary  ar- 
teries, when  the  muscular  pressure  is  greatest  07t  them  (in 
systole),  for  at  the  moment  of  greatest  pressure  tbdr 


32  V  PERICARDITIS. 

mouths  are  closed  and  held  closed  by  a  force  equivalent 
to  that  very  pressure. 

Mr.  Geo.  C.  Karop  says  {N.  Y.  Med.  Jour.,  July  7, 
1883)  that  while  the  best  authorities  are  divided,  some 
asserting,  some  denying  that  the  coronary  arteries  an- 
astomose, when  junior  Demonstrator  of  Anatomy  at 
Middlesex  Hospital,  he  made  some  injections,  and  found 
that  in  some  cases  they  anastomosed,  and  in  others  they 
did  not,  the  latter  being  as  two  to  one. 

The  question  requires  further  attention,  "  but  the  con- 
clusion will  probably  remain  as  before,  that  in  some  cases 
the  anastomosis  is  very  free,  in  some  slight,  and  in  others 
does  not  occur  at  all.'* 


LECTURE   II. 

PERICARDITIS. 

The  pericardium  is  the  sac  or  bag  about  the  hearty 
containing  it.  It  is  double  in  two  senses.  The  real  sac 
is  made  up  of  two  structures  or.  tissues.  The  outside  one 
is  formed  of  fibrous  tissue,  not  unHke  that  which  forms 
the  ligaments  of  the  joints,  but  less  condensed,  and  is 
continuous  with  cordiform  tendon  of  the  diaphragm 
below,  and  the  outer  covering  of  the  large  vessels  above. 
The  inner  layer  is  a  serous  membrane,  no  more  and  no 
less  incorporated  by  interchange  of  fibres  with  the  outer 
layer,  so  that  it  cannot  be  separated  by  the  scalpel  without 
considerable  labor.  These  two  constitute  the  heart  sac. 
From  this,  at  or  near  the  origin  of  the  great  vessels,  the 
inner  or  serous  layer  is  continued  on  to  the  heart  and 
wholly  invests  it,  forming  a  closely  adhesive  layer.  Serous 
membranes  everywhere  are  constructed  on  the  same  plan, 


PERICARDITIS.  33 

lining  the  parietes  and  covering  the  viscus  without  break 
of  continuity. 

The  term  pericarditis  is  used  to  designate  the  inflam- 
mation of  this  serous  lining  of  the  fibrous  pericardium 
and  this  serous  covering  of  the  heart. 

Here,  when  we  have  to  use  percussion  as  a  means  of 
diagnosis,  is  as  good  a  place  as  any  to  give  an  explana- 
tion of  a  method  by  which  the  auscultation  of  percussion 
is  in  certain  respects  improved  —  into  which  a  new 
principle  is  introduced.  The  percussion  of  Laennec  gives 
information  regarding  the  condition  of  the  different 
organs  of  the  body  by  the  greater  or  less  volume  of 
sound,  and  by  modification  in  the  tone  of  sound  pro- 
duced by  it.  This  results  from  vibrations  produced  in 
the  cov'ering  structures,  and  will  be  freer  and  of  deeper 
note  if  air  or  gas  or  a  rarefied  structure  be  underneath, 
but  of  higher  pitch  and  scanty  volume  if  a  solid  body  or 
fluid  be  in  contact  with  the  percussed  surface.  Every 
carpenter  in  the  land  understands  the  practice  growing 
out  of  this  principle  and  applies  it  when  he  is  to  drive  a 
nail  into  the  plastered  wall  of  a  room.  He  taps  with  a 
light  hammer  on  the  wall  from  side  to  side  till  he  strikes 
a  spot  where  he  finds  the  sound  is  not  *' hollow"  and  is  of 
less  volume,  and  he  knows  that  he  has  found  a  timber 
that  "will  hold  his  nail."  Persons  keeping  fluids  in 
wooden  casks  apply  the  same  principle  to  ascertain  how 
much  fluid  is  left  in  them.  The  farmer  strikes  the  cider 
barrel  with  his  knuckle,  from  above  downward.  At  first 
the  sound  produced  is  clear  and  free,  and  soon  it  is 
suddenly  changed  in  volume  and  tone.  He  knows  that 
is  the  cider  level.  The  sound  in  all  these  cases  is  pro- 
duced in  the  containing  wall. 

In  the  year  1840,  probably  in  January,  the  late  Dr. 
Cammann  called  on  me  with  a  new  idea.  It  was  no  more 
than  a  thought.     He  had  not  attempted  to   prove   or 


34  PERICARDITIS. 

apply  it.  May  not  vibrations  be  produced  in  solid  or 
thick  walled  organs  which  can  be  brought  to  the  ear  as 
sound?  He  had  no  sooner  stated  his  point  than  I  saw, 
or  thought  I  saw,  a  new  field  of  useful  investigation.  We 
agreed  at  once  to  give  our  leisure  time  to  the  inquiry. 
We  met  day  after  day  at  the  dead  house  of  Bellevue 
Hospital,  where  I  was  already  an  accepted  volunteer,  and 
with  stethoscopes  of  solid  cedar  wood,  one  inch  in 
diameter,  and  six  inches  long,  or  wedge-shape,  or  almost 
pointed  at  the  objective  extremity,  each  furnished  with 
an  ivory  ear-rest  through  which  the  cedar  projected 
slightly,  we  began  and  prosecuted  the  study.  Dr.  C.  S. 
Mitchell,  then  of  New  York,  now  of  Brooklyn,  often  met 
with  us  and  gave  us  his  assistance.  The  m.ode  of  pro- 
ceeding was  this :  The  objective  end  of  the  stethoscope 
was  in  central  position  over  the  heart,  for  example,  or 
over  the  spot  where  the  lung  does  not  overlap  it,  and  the 
ear  was  applied  to  the  aural  end,  leaving  the  two  hands 
free.  The  forefinger  of  left  hand  was  the  pleximeter,  and 
the  first  two  of  the  right  the  hammer.  By  standing  on  the 
right  side  of  the  body,  and  then  on  the  left,  we  could 
easily  percuss  in  the  whole  circumference  of  the  heart. 
We  percussed  first  off  the  heart  and  made  the  percussion 
approach  it  in  a  right  line  on  every  side  in  succession. 
While  the  percussion  had  not  reached  the  organ,  the 
sound  was  distant  and  of  small  volume;  but  when  it 
reached  the  outer  border  of  it,  on  either  hand,  the  sound 
grew  instantly  louder  and  acquired  a  half  metallic  ring. 
This  point  was  accurately  marked.  In  this  way  the  whole 
circumference  was  mapped  out,  and  then  sharpened 
knitting  needles  were  driven  into  the  chest,  at  these 
marked  spots,  perpendicular  to  the  plane  of  the  body.  We 
were  surprised  at  the  accuracy  of  our  measurements. 
The  needles  were  always  in  contact  with  the  pericardium, 
often  entering  it  without  wounding  the  heart.     Tkese 


,  PERICARDITIS.  35 

experiments  were  repeated  day  after  day  by  ourselves 
and  by  friends,  and  always  with  the  same  results.  Upon 
the  dead  body,  then,  the  demonstration  was  complete. 

We  tried  the  same  method  for  fixing  the  boundaries  of 
the  liver,  the  spleen,  and  the  kidneys,  and  found  it  equally 
accurate  on  them,  with  this  exception,  that  the  liver  was 
the  least  conductive  of  them  all,  but  that  the  limits  of 
this  could  be  easily  defined  when  the  stethoscope  was  not 
more  than  two  inches  and  a  half  from  the  border. 

These  facts  and  others  of  the  same  kind  were  arranged 
for  publication  by  myself,  and  appeared  in  the  July  num- 
ber, 1840,  of  a  journal  edited  by  Drs.  Watson  and  Swift. 

Soon  after  this  paper  appeared,  a  meeting  of  the  New 
York  Medical  and  Surgical  Society  was  held  in  the 
Library  of  the  New  York  Hospital,  and  a  patient  was 
brought  in  on  whose  chest  the  boundaries  of  the  heart 
had  been  marked  by  an  ink  line,  and  the  members,  one 
after  another,  tried  the  new  method,  and,  as  I  now  re- 
member, each  member  indicated  the  same  line,  some  at 
once,  some  after  a  second  trial  and  some  hesitation.  I 
state  this  to  show  that  the  art  of  this  plan  is  not  difficult 
of  acquisition. 

My  lamented  friend  Dr.  Powers,  of  Baltimore,  soon  after 
reading  the  paper,  was  called  to  see  a  patient  who  carried 
a  large  abdominal  tumor,  the  nature  and  relations  of 
which  were  not  determined.  He  could  not  himself  per- 
cuss anteriorly  and  listen  behind;  another  percussed  for 
him,  and  he  carried  the  stethoscope  from  near  the  point 
of  percussion  backward  to  the  usual  place  of  the  kidney 
of  that  side,  and  finding  no  break  of  continuity,  only 
a  uniformly  diminishing  volume,  he  pronounced  the 
kidney  and  the  tumor  continuous  structures.  The  size 
of  the  tumor  rendered  this  opinion  improbable,  but 
inspection  after  death  proved  it  to  be  correct. 

Not  long  ago  a  gentleman  was  brought  to  me  from  the 


36  PERICARDITIS, 

West  by  his  physician,  who  was  not  satisfied  with  the 
term  malignant  which  had  been  applied  by  a  surgeon  to 
an  apparent  tumor  in  the  right  side  of  the  abdomen,  and 
much  less  with  the  surgeon's  proposition  to  remove  it. 
I  found  it  movable,  and  especially  that  it  could  be  pressed 
upward  and  backward  toward  the  place  the  kidney  should 
occupy,  but  particularly  on  placing  the  patient  in  a 
horizontal  position,  his  elbows  on  a  chair.  I  found,  by 
auscultatory  percussion,  that  there  was  no  organ  where  the 
kidney  should  be  to  give  any  sudden  change,  at  its 
borders,  to  the  percussion  sound.  On  these  two  facts 
was  based  the  opinion  that  the  *' tumor"  was  a  floating 
kidney.  I  am  not  informed,  and  may  never  be,  whether 
this  opinion  was  correct. 

Last  winter  a  large  consultation  of  the  Me<iical  Board 
of  St.  Luke's  Hospital  was  called  to  decide  on  the  pro- 
priety of  removing  what  appeared  to  be  a  diseased  kid- 
ney. Auscultatory  percussion  was  tried  in  that  case,  the 
stethoscope  being  placed  over  the  kidney  and  percussion 
made  from  it  toward  the  right  (it  was  the  left  kidney), 
and  it  was  found  that  the  peculiar  percussion  note  ceased 
where  the  right  limit  of  the  kidney  should  be,  and  was  not 
renewed  when  percussion  was  made  on  the  tumor.  It 
was,  therefore,  stated  that  the  kidney  had  no  structural 
connection  with  the  tumor,  and  the  haematuria  which  had 
been  a  misguiding  symptom  might  come  from  the 
extension  of  the  malignant  disease  of  the  tumor  to  the 
ureter.  This  opinion,  suggested  mainly  by  the  stetho- 
scope and  percussion  combined,  was  proved  to  be 
minutely  correct  at  the  examination  after  death. 

Auscultatory  percussion  may  be  practised  on  all  organs 
to  which  it  is  applicable,  in  the  same  way  as  it  was  on 
this  kidney.  The  information  given  by  losing  the  per- 
cussion note  is  of  the  same  import  as  that  given  by  find- 
ing it,  and  gives  equally  reliable  information  regarding 


PERICARDITIS.  37 

i 

the  limits  of  organs.  This  is  true  even  of  the  liver  if 
the  stethoscope  is  not  placed  too  far  from  the  border  to 
be  examined. 

There  is  another  mode  of  using  the  stethoscope  and 
percussion  together  which  is  explained  on  a  similar 
principle.  The  instrument  may  be  placed  entirely  off 
from  the  organ  under  examination,  and  at  a  distance 
of  two  or  three  inches  from  it,  and  percussion  made  first 
on  the  organ  and  toward  the  instrument.  When  the  per- 
cussion passes  off  the  organ  a  new  and  sharper  note  is 
heard.  This  is  more  true  of  the  chest  than  of  other 
parts,  because  the  walls  of  the  chest  are  more  fixed  and 
more  conductive.  For  example,  the  percussion  sound 
from  the  heart  when  the  instrument  is  placed  an  inch  or 
two  from  it  is  dull  and  distant,  and  as  the  percussion 
passes  off  its  border  it  becomes  sharp  and  clear.  The 
percussion  vibrations  are  taken  by  the  muscles  and 
tissues  of  tile  chest  walls,  while,  so  far  as  the  heart 
extends,  these  vibrations  are  more  or  less  stifled  and 
smothered. 

I  have  made  this  digression  in  favor  of  auscultatory 
percussion  because  I  do  not  believe  the  knowledge  of 
that  mode  of  examination  is  at  all  general  in  the  pro- 
fession, although  I  have  explained  it  every  year  to  medical 
classes  since  the  paper  was  published.  The  journal  in 
which  it  appeared  did  not  survive  its  first  year,  killed 
outright  by  a  review  from  the  pen  of  one  of  its  editors, 
and  has  been  seen  no  more.  I  have  been  told,  however, 
that  it  received,  at  the  time,  the  distinction  of  being 
translated  into  another  language  and  published  in  an 
undistinguished  medical  journal,  the  authors'  names 
suppressed  and  the  translator's  name  appearing  in  their 
place.  I  have  not  seen  this  translation  and  theft;  my 
informant  said  that  he  had.  Any  way  it  appears  that 
there  are  few  either  here  or  abroad  that  know  anything 


38  PERICARDITIS, 


about  the  matter;  perhaps  none  now  practice  it  except 
those  who  have  listened  to  my  lectures. 

As  to  the  form  of  stethoscope,  that  already  described 
is  probably  the  best,  but  any  stethoscope  will  answer  the 
purpose.  I  have  often  gone  back  to  the  primal  instru- 
ment of  Laennec,  a  rolled  pamphlet,  when  a  better  was 
not  at  hand. 

In  its  application  to  the  heart  of  a  living  person  the  indi- 
cations are  not  always  as  satisfactory  as  in  the  dead  body. 
The  reasons  for  this  are — ist,  That  in  the  latter  the  lungs 
are  in  the  position  of  rest,  i.e.,  expiration ;  and  2nd,  that 
the  depth  of  lung  overlying  the  heart  in  the  living  is 
constantly  changing,  in  inspiration  more,  in  expiration 
less ;  and  then  the  depth  of  lung  over  the  heart  varies  in 
different  persons,  and  may  make  the  exploration  easy  in 
one  and  difficult  in  another.  In  case  of  difficulty  it  will 
be  well  to  have  the  patient  make  a  full  expiration  and 
suspend  the  breathing  for  a  few  seconds  while  the 
physician  percusses ;  or  the  latter  may  place  the  instru- 
ment an  inch  or  more  away  from  the  probable  place  of 
the  border  of  the  organ  and  percuss  toward  it  from  the 
heart. 

There  is  another  point  to  be  made :  the  ribs  are  excel- 
lent conductors  of  sound,  much  better  than  the  tissues  of 
the  intercostal  spaces ;  if,  therefore,  the  instrument  be 
placed  on  a  rib  or  cartilage  and  percussion  is  made  on  the 
same  rib,  the  sound  may  seem  to  indicate  a  much  greater 
size  of  the  heart  than  is  real.  If,  then,  the  instrument 
rests  on  a  rib  the  percussion  should  be  made  above  or  be- 
low that  rib,  or  the  intercostal  stethoscope  may  be  used, 
which  is  wedge  shape,  and  applied  so  as  not  to  touch  any 
rib.  The  stethoscope  that  tapers  down  from  an  inch 
in  diameter  at  its  aural  extremity  to  \  of  an  inch  at 
the  applied  end  will  serve  equally  well,  although  this 
was  devised  for  the  purpose  of  detecting  small  deposits 


PERICARDITIS.  39 

of  solid  structure  or  thickened  tissue  anywhere  in  the 
body. 

With  these  cautions  and  helps  it  will  be  in  only  a  very 
exceptional  case  that  the  observer  cannot  make  out  the 
position  and  boundaries  of  the  heart  with  accuracy.  He 
will,  of  course,  confirm  the  indications  given  by  the  steth- 
oscope by  those  discoverable  from  ordinary  percussion 
and  the  point  of  the  apex  beat. 

The  result  of  this  work  thus  detailed,  so  far  as  the 
heart  is  concerned,  was  to  show  that  its  upper  boundary 
was  the  upper  border  of  the  left  third  rib,  and  this  line 
extended  across  the  sternum,  while  the  left  auricle  rose 
into  the  second  left  intercostal  space  when  filled;  and 
the  right,  extending  half  an  inch  from  the  sternum  to  the 
right,  when  in  a  like  condition — that  the  left  boundary 
was  a  curved  line  beginning  on  the  third  rib  three  inches 
from  the  median  line — on  the  fourth  rib  four  inches,  and 
in  the  fifth  intercostal  space  3^-  inches. 

Morbid  Anatomy. — In  acute  pericarditis  there  is  doubt- 
less the  same  congestion  of  the  blood-vessels  that  is  ob- 
served in  the  first  stage  of  other  serous  inflammations, 
though  little  of  it  is  seen  when  the  disease  has  run  its 
course.  There  is,  in  all  probability,  in  all  cases,  some 
production  of  pus,  though  commonly  not  enough  to  be 
seen  by  the  unaided  eye.  This  seems  to  be  a  common 
event  in  serous  inflammations  and  perhaps  in  all  inflam- 
mations, and  is  regarded  as  due  to  the  transition  of  the 
white  corpuscles  of  the  blood  through  the  walls  of  capil- 
lary vessels.  Cohnheim  first  saw  these  bodies  working 
their  way  through,  and  appearing  on  the  outside  of  these 
vessels,  and  thought  he  recognized  their  identity  with  the 
pus  corpuscles.  This  observation  has  been  confirmed  by 
many  workers  with  the  microscope. 

The  red  corpuscles  of  the  blood  sometimes  break 
bounds  in  the  same  way  and  stain  the  other  effusions. 


40  PERICARDITIS. 

But  this  does  not  occur  in  visible  quantity  except  when 
pericarditis  occurs  in  persons  already  affected  with  scurvy, 
or  in  persons  whose  condition  is  allied  to  that  prevailing 
in  that  disease.  Then  the  quantity  of  blood  may  be  con- 
siderable and  the  disease  is  called  hemorrhagic  pericar- 
ditis. In  this  condition  if  persons  are  attacked  by  this 
disease  or  by  pleurisy,  it  is  pretty  safe  to  infer  that  it  is 
hemorrhagic.  A  prisoner  for  some  misconduct  was  put 
on  a  diet  of  bread  and  water.  This  discipline  diet  was 
continued  for  some  weeks,  and  the  man  was  much  re- 
duced by  it.  In  this  state  he  was  brought  to  bed  by  per- 
icarditis, and  sent  to  the  hospital.  I  assumed  that  it  was 
the  hemorrhagic  form,  not  from  any  peculiar  behavior  of 
the  disease,  for  it  has  no  distinctive  symptoms,  but  from 
the  man's  history  and  condition ;  and  so  it  was.  In  a 
hundred  cases  occurring  under  ordinary  circumstances  no 
blood  will  be  seeyi. 

The  common  effusions  are  fibrine  and  serum.  The 
first  clinically  recognizable  is  the  fibrine.  A  day  or  two 
later  the  fluid,  if  it  become  at  all  abundant,  can  be  found. 
The  appearance  of  the  fibrine  is  variable.  In  one  person 
it  may  be  spread  as  a  thin,  smooth  membrane  over  all 
the  inner  face  of  the  pericardial  sac  and  the  outer  surface 
of  the  heart.  In  another  it  is  more  abundant,  and  ap- 
pears to  have  caused  attachment  of  the  pericardium  to 
the  heart,  but  afterward  these  surfaces  are  separated  by 
the  interposition  of  serum,  and  a  part  of  the  fibrine  is  seen 
attached  to  one  surface  and  a  part  to  the  other.  In  rare 
cases  this  division  of  the  fibrine  between  the  heart  is 
pretty  even,  giving  to  each  nearly  an  equal  share.  Then 
it  may  be  found  that  many  little  threads  of  fibrine  run 
through  the  fluid  from  one  division  to  the  other,  looking 
like  little  pillars.  But  much  more  frequently  the  division 
is  very  unequal  and  is  complete.  Then  the  surfaces  of 
the  effusion  may  be  very  rough.     On  one  side  lumps  of 


PERICARDITIS. 


41 


irregular  shape  may  be  left,  corresponding  with  dents 
or  depressions  on  the  other,  or  the  heart  may  be  partly 
covered  by  little  cones  or  nipples,  and  the  pericardial  sur- 
face be  left  nearly  without  fibrine.  This  latter  arrange- 
ment was  once  thought  to  be  significant,  and  had  the  epi- 
thet "scabrous"  attached  to  it.  But  it  was  regarded  as 
indicating  nothing  as  to  the  nature  of  the  inflammation. 
It  is  evident  that  when  serum  is  effused  after  the  fibrous 
membrane  is  formed  it  finds  a  place  for  itself,  when  this 
new  membrane  will  most  easily  yield  to  it,  and  that 
this  effusion  is  more  firmly  attached  to  living  membrane 
than  to  itself,  and  is  more  easily  split  into  layers  than 
detached.  The  mode  of  separation  is  of  little  importance 
when  it  is  properly  understood. 

The  quantity  of  serum  in  acute  pericarditis  varies 
greatly.  Often  there  is  so  little  of  it  that  its  presence  is 
hardly  appreciable  during  life  and  appears  insignificant 
after  death,  but,  in  most  cases,  it  is  found  in  the  sac  to 
amount  to  a  few  ounces  or  even  to  a  pint  or  more. 

The  sequel  of  the  plastic  effusion  is  important  if  the 
patient  recovers.  During  recovery  it  seals  the  pericar- 
dium firmly  to  the  heart,  so  that  if  the  patient  dies  months 
after  the  pericardial  inflammation  has  passed  away  the 
adhesion  is  still  found,  though  in  the  mean  time  the  pa- 
tient thought  he  was  well,  and  acted  like  a  well  man,  but 
the  time  will  come  if  the  patient  live  long  enough  when 
the  separation  will  be  complete.  A  child  of  six  years 
had  rheumatism  and  pericarditis  under  the  care  of  Dr. 
Smith  of  Randolph,  Vt.  He  grew  to  be  a  man,  and  was 
an  industrious  and  useful  man.  He  died  at  the  age  of 
twenty-eight,  and  here  is  his  heart.  You  will  see  that 
the  pericardium  is  attached  to  the  heart,  not  in  close  ad- 
hesion, but  by  countless  numbers  of  small  threads  half 
an  inch  or  so  in  length.  The  spaces  between  the  attach- 
ment of   the  threads   show  healthy  pericardium.      The 


42  PERICARDITIS. 

next  step  will  be  the  rupture  or  absorption  of  these 
threads.  If  it  is  true  that  ''old  Pan"  had  a  "hairy- 
heart, "  it  must  be  explained  by  the  supposition  that 
these  threads  were  found  broken  but  not  wholly  ab- 
sorbed ;  consequently  that  he  had  had  pericarditis. 

The  evil  caused  by  this  adhesion  can  be  best  under- 
stood by  referring  again  to  anatomy.     If  you  dissect  a 
heart,  say  a  bullock's  heart  that  has  been  boiled,  you  will 
easily  see  the  muscular-bands  running  in  almost  every  di- 
rection and  one  layer  in  contact  with  another,  and  partic- 
ularly you  will  find  a  band  beginning  at  the  base  of  the 
heart,  and  running  obliquely  downward  and  to  the  left 
till  it  comes  near  to  the  apex,  when  it  makes  a  corkscrew 
turn  about  this  part  of  the  organ.     The  effect  of  this  is 
to  draw  the  apex  forward  with  each  beat.     This  explains 
the  fact  that  when  this  organ  is  healthy  we  feel  the  apex 
beat  easier  than  that  of  any  other  part  of  it.     It  implies, 
also,  a  twisting  movement  of  the  apex  in  the  heart-sac — 
a  movement  easily  performed  when  there  are  no  adhe- 
sions, but  resisted  when  the  pericardium  is  adherent  by 
the  attachment  of  the  latter  to  the  cordiform  tendon  of 
the  diaphragm.     You  would  naturally  infer  from  this  that 
as  more  strength  is  needed  the  need  would  be  supplied 
by  more  strength  in  the  heart,  in  other  words,  by  hyper- 
trophy.    But  here  I  show  a  heart  on  which  the  pericar- 
dium is  completely  attached  in  every  part,  and  had  been 
so  for  twelve  months  before  death,  and  there  is  no  hyper- 
trophy whatever.     The  attaching  membrane  is  very  thin 
and  delicate.      But  here  is  one  in  the  same  condition, 
except  that  the  intervening   material  is  very  thick  and 
stiff,  and  does  not  seem  to  be  fully  organized,  the  new 
membrane  having  a  leathery  character,  and  must   have 
been  in  itself  an  obstacle  to  the  heart's  action,  yet  even 
here  the  heart  is  not  hypertrophied.     On  this  tray  I  show 
you  several  specimens  illustrating  the  same  thing.     The 


PERICARDITIS.  43 

rule,  then,  seems  to  be  that  simple  adhesions  of  the  peri- 
cardium to  the  heart  do  induce  enlargement  of  that 
organ.  And  I  do  not  remember  any  exceptions.  The 
rule  is  very  different,  as  you  will  see  by  and  by,  when 
the  valves  of  the  part  are  implicated. 

One  remark  forces  itself  upon  me  here.  In  some  of 
the  serous  inflammations  it  seems  to  be  demonstrated  that 
there  are  little  granules  of  .connective  tissue  cells  studding 
most  of  the  inflamed  surface,  and  that  the  granules  and 
not  false  membranes  are  the  agents  of  attachments  and 
adhesions,  while  the  false  membranes  become  fatty  and 
are  absorbed.  In  many  of  the  hearts  you  are  now  examin- 
ing I  admit  that  in  their  present  state  we  cannot,  on  them, 
disprove  this  theory,  but  how  is  it  with  that  one  in  which 
the  new  material  is  nearly  an  eighth  of  an  inch  in  thick- 
ness ?  Is  it  possible  that  adhesion  is  by  agency  of  such 
granules  ?  The  fleecy  appearance  in  the  central  layer  of 
this  shows  that  the  false  membrane  is  still  there. 

There  is  one  thing  more  to  be  said  while  on  the  pathology 
of  pericarditis.  Here  is  a  heart  to  which  the  pericardium 
is  firmly  attached  on  the  left,  while  it  is  separated  from 
the  right  side  and  greatly  distended  or  bulged.  It  is  from 
a  person  about  twelve  years  of  age,  who  for  several  suc- 
cessive years  had  an  attack  of  rheumatism  in  the  spring, 
attended  almost  every  time  with  pericarditis.  The  last 
was  attended  by  some  oedema,  great  cyanosis  and  dis- 
tressing dyspnoea.  There  was  marked  extension  of  peri- 
cardial dulness,  especially  to  the  right.  This  heart  was 
found  in  the  condition  in  which  you  see  it,  except  that 
the  distended  part  of  the  pericardium  contained  a  large 
quantity  of  serous  fluid,  which  so  pressed  upon  and  com- 
pressed the  right  heart  as  at  length  to  make  the  circula- 
tion impossible.  The  inference  is  that  when  the  last 
attack  of  pericarditis  began  the  adhesions  were  over  all 
the  heart,  and  that  the  force  of  the  new  effusion  separated 


44  PERICARDITIS. 

the  attachments  so  far  as  they  are  separated,  and  that 
the  adhesions  elsewhere  were  too  firm  to  yield  to  it. 
Your  own  examination  will  show  you  that  what  remain 
are  very  firm. 

In  cases  in  which  there  are  no  previous  adhesion  the 
amount  of  serous  effusion  is  very  large  and  very  distress- 
ing. This  will  be  referred  to  when  speaking  of  symp- 
toms. 

In  chronic  pericarditis  there  is  always  an  abundant 
seropurulent  effusion,  and  the  pericardium  is  much  thick- 
ened. 

Causes. — Pericarditis  does  occur  sometimes  as  an  inde- 
pendent disease,  but  it  is  almost  always  secondary  to  or 
at  least  co-existent  with  some  other  disease  ;  for  example, 
Dr.  Latham  had  in  four  years  at  St.  Bartholomew's  Hos- 
pital 136  cases  of  acute  rheumatism,  in  which  he  found 
the  heart  affected  in  90,  the  endocardium,  however, 
oftener  than  the  pericardium,  i.e.,  in  74 — the  pericardium 
in  18.  Another  observer  gives  an  analysis  of  1410  cases 
of  all  diseases.  There  were  in  this  number  161  who 
had  acute  rheumatism.  Of  the  1410,  85  had  recent  peri- 
carditis— 61  in  the  rheumatic  cases,  i  in  3,  say,  and  24 
among  patients  that  had  not  rheumatism.  Of  his  24 
cases  not  rheumatic  7  followed  inflammation  of  the  lungs 
or  pleura  ;  2,  malignant  disease  of  the  heart ;  I,  old  cardiac 
disease — 6  were  connected  with  granular  kidney;  4  fol- 
lowed hemorrhage  and  exhaustion  ;  2,  scarlet  fever  and 
erysipelas,  and  2  were  not  explained  by  any  preceding  or 
attendant  disease.  Dr.  John  Taylor  found  pericarditis  of 
a  severe  grade,  in  i  out  of  every  80  cases  in  the  Univer- 
sity College  Hospital,  and  of  these  about  two  thirds 
occurred  in  the  progress  of  acute  rheumatism.  The  con- 
nection between  pericarditis  and  acute  rheumatism  was 
established  by  Bouillaud,  though  partly  seen  by  several 
persons  before  him.     Perhaps  the  first  person  who  recog- 


PERICARDITIS.  45 

nized  the  fact  that  acute  rheumatism  can  produce  "  disease 
of  the  heart"  was  Dr.  Smith  of  Randolph,  Vt.,  in  a  case 
to  be  spoken  of  hereafter.  In  persons  suffering  from 
Bright's  disease,  whether  it  be  the  variety  known  as  the 
large  white  kidney,  or  the  contracted  granular  kidney,  a 
certain  number  contract  acute  pericarditis.  Dr.  Latham, 
as  I  have  told  you,  had  6  cases  of  this  kind  in  85.  Dr. 
Taylor  in  his  35  cases,  ascribes  one  third  to  Bright's 
disease. 

The  relations  of  acute  pericarditis  and  pneumonia 
deserve  attention.  In  fifty  years  of  attendance  on  hospi- 
tals in  one  capacity  or  another,  I  have  been  many  times 
surprised  to  find  acute  pericarditis  in  persons  who  were 
supposed  to  have  died  of  pneumonia  alone.  This  did  not 
arise  from  any  real  difficulty  in  diagnosis,  but  from  the 
fact  that  the  symptoms  appeared  to  all  accounted  for  by 
the  recognized  pneumonia,  and  no  search  was  made  for 
any  complication.  The  pericarditis  is  as  easily  recognized 
in  this  connection  as  under  any  circumstances.  After 
several  such  surprises  I  adopted  the  practice  of  listening 
for  the  heart  disease  in  every  case  of  pnenmonia.  Dr. 
Latham  had  7  concurrent  with  this  disease  and  pleurisy 
together. 

As  to  the  relations  of  acute  pericarditis  and  scarlet 
fever,  I  do  not  remember  any  instance  in  which  the  heart 
disease  has  occurred  in  the  stage  of  eruption,  but,  with 
me,  it  has  occurred  several  times  in  the  oedema  that  is  a 
frequent  sequel  of  it. 

Pericarditis  may  be  caused  by  inflammation  beginning 
in  neighboring  tissues,  and  by  abscess  of  such  parts  open- 
ing into  it.  In  the  latter  case  the  inflammatory  effusion 
is  pus  and  fibrine.  So  it  is  if  the  disease  occur  in  the 
course  of  pyaemia.  A  singular  case  of  purulent  pericardi- 
tis will  be  narrated  by  and  by,  artificial  teeth  and  the  plate 
on  which  they  were  set  having  passed  into  the  oesophagus. 


4-6  PERICARDITIS. 

The  white  hard  patches  so  often  found  on  the  anterior 
face  of  the  heart,  often  called  "milk  spots,"  are  regarded 
as  of  inflammatory  origin,  although  during  life  no  symp- 
toms of  inflammatory  action  have  been  noticed.  They 
are  composed  of  fibres  like  those  of  the  connective  tissue, 
and  acquire  a  firmness  and  hardness  that  is  not  observed 
in  that  tissue  while  in  a  healthy  state.  When  old  they 
may  become  calcareous. 

The  serous  membranes  throughout  the  body  are  nour- 
ished by  vessels  on  their  attached  surfaces,  branches  of 
which  penetrate  the  structures  covered  by  them.  It  is  not 
surprising,  therefore,  that  those  structures  should  partake 
of  diseased  action  that  is  begun  in  the  membrane. 
Hence,  when  pericarditis  is  acute  and  fatal  it  is  not 
uncommon  to  find  an  oedema  of  the  outer  layer  of  the 
heart  fibres,  a  paler  color  and  softening.  This  will  natu- 
rally diminish  in  some  degree  the  force  of  the  heart-con- 
tractions during  life.  This  is  a  limited  carditis  secondary 
to  the  pericarditis. 

The  symptoms  of  pericarditis  are  very  vague  and  ob- 
scure. It  often  cannot  be  made  out  without  the  physical 
signs,  consequently  little  was  known  of  it  except  its  post 
^nortem  manifestations,  till  the  rules  of  auscultation  and 
percussion  were  systematized.  There  may  be  a  sense  of 
weight  and  oppression  in  the  chest.  There  will  be  an  in- 
creased frequency  of  pulse  and  respiration.  There  may 
be  a  painful  sensation  produced  by  pressure  in  an  inter- 
costal space  over  the  heart,  or  pressing  the  liver  upward 
by  the  finger  under  the  ribs,  at  or  to  the  left  of  the  epi- 
gastrium, but  of  unprovoked  or  spontaneous  pain  there 
is  none  or  next  to  none. 

We  turn,  then,  to  the  physical  diagnosis,  which  is 
always,  or  almost  always,  complete.  For  this  purpose  it 
is  desirable  to  consider,  first,  the  cases  in  which  the  fibrin- 
ous exudation  is  the  principal,  or,  perhaps,  the  only  in- 


PERICARDITIS.  47 

flammatory  product.     These  cases  are  known  as  dry  peri- 
carditis.    The  second  class  of  cases  comprises  those  in 
which,   though  there  is,  perhaps,   the   usual   amount  of 
fibrine  produced,  the  prevailing  exudation  is  serum.     In 
both  of  these  classes  there  is  probably  an  initiatory  fric- 
tion sound  due  to  the  dry  state  of  the  pericardium  dur- 
ing the  inflammatory  congestion,  which  precedes  the  exu- 
dation.    Dr.  Stokes,  a  great   many  years   ago,  reported 
such  a  sound,  and  on  his  authority  I  readily  believe  in  its 
existence,  although  I  have  never  heard  it.     And  yet  it 
seems  to  me  strange  that  it  should  have  escaped  me;  I 
have  so  often  listened  in  acute  rheumatism  for  the  com- 
ing of  the  cardiac  complication.     In   some  of  the  many 
hundred  cases  of  this  kind,  spread  through  half  a  century, 
it  strikes  me  that  I  ought  to  have  heard  it ;  but  I  must 
say  that   I   have   not.     When   the   serum   or  liquor  san- 
guinis escapes  from  the  vessels  these  will  act  as  a  lubri- 
cant and  extinguish  this  rubbing  till  the  fibrine  is  coagula- 
ted in  the  latter,  then  a  new  friction  sound  is  developed 
by  the  fibrine.     This  friction  is  at  first  heard  in  the  con- 
traction of   the  heart.     A  few  hours  to  a  day  later  it 
becomes  double,  being  heard  in  systole,  and  repeated  in 
diastole.     Commonly  the  first  of  these  friction  sounds  is 
more   distinct  than   the  second,  though  both  are  easily 
recognized.     This  is,  doubtless,  due  to  the  greater  force 
of  the  systolic  action,  at  first  causing  sound  with  a  smaller 
quantity  of  fibrine  than  is  recognized  by  the  diastole,  and 
afterwards  showing  the  preponderance  due  to  its  strength. 
The  fact  that  the  friction  sound  is  first  single  and  then 
double  is  of  the  first  importance.     Any  physician,  young 
or  old,  may,  when  he  listens  for  the  first  time  to  a  par- 
ticular patient  and  finds  an  abnormal  sound,  doubt  whether 
the  sound  is  produced  by  a  valvular  change  or  external 
friction,  or  as  Dr.  Latham  would  have  said,  whether  the 
sound  is  "exocardial"  or  "endocardial,"  and  generally 


48  PERICARDITIS. 

the  tone  of  these  sounds  is  not  so  characteristically  dis- 
tinct as  to  base  an  opinion  on  difference  between  them. 
But  there  is  no  endocardial  murmur  that  can  be  single  to- 
day and  double  to-morrow.  This  peculiarity  belongs  to 
the  exocardial  or  friction  sound.  The  changes  in  the 
form  of  the  valves  that  produce  murmurs  are  slow,  grad- 
ual, and  in  acute  endocarditis  if  a  murmur  is  produced  at 
all  it  is  never  double  till  weeks  and  sometimes  months 
have  elapsed  from  the  time  of  the  attack.  The  fact  then 
that  the  abnormal  sound  was  single  yesterday,  that  is,  one 
sound  for  one  heart  beat,  and  is  double  to-day,  one  sound 
in  systole  and  another  in  diastole,  is  all  but  diagnostic  of 
acute  pericarditis. 

But  if  the  physician  does  not  see  the  patient  till  the 
friction  gives  a  double  sound,  how  then  ?  There  are 
double  endocardial  murmurs  occurring  in  the  same  times 
as  the  exocardial  friction  sounds.  If  the  sounds  are  endo- 
cardial the  history  of  the  patient  will  be  important ;  if  he 
has  rheumatism,  has  he  had  it  previously?  Has  ascending 
or  active  exercise  produced  unusual  shortness  of  breath? 
Is  the  heart  enlarged  ?  You  may,  even  if  there  is  fluid 
effusion  in  the  pericardium,  answer  this  last  question  by 
the  aid  of  auscultatory  percussion.  In  a  Word,  has  the 
patient  had  heart  disease  previous  to  this  sickness  ?  If 
he  has  not,  the  presumption  is  in  favor  of  pericarditis.  If 
he  has  chronic  disease  of  valves  and  double  murmur,  the 
tone  of  the  sound  may  be  distinctive  or  it  may  not.  The 
tones  of  old  valvular  disease  vary  very  much  ;  sometimes 
the  sound  resembles  that  produced  by  sawing;  sometimes 
that  of  filing,  or  rasping.  If  the  sounds,  one  or  both  are 
harsh  they  are  not  the  sounds  of  friction ;  if  they  are 
of  softer  tone  but  harsher  than  the  breathed  "  a-w-e,"  they 
may  be  produced  either  within  or  on  the  outside  of  the 
heart ;  if  it  is  blowing,  it  is  probably  endocardial. 

The  friction  sound  is  of  a  pretty  uniform  tone  when 


PERICARDITIS.  49 

heard  in  different  persons.  It  was  called  by  him  who 
first  described  it  the  noise  of  new  leather,  but  it  is  not 
nearly  so  coarse  or  harsh  as  that.  The  sound  caused  by 
placing  the  palm  of  one  hand  over  the  ear  and  rubbing 
the  back  of  that  hand  with  the  finger  of  the  other  is  a 
nearer  approach  to  it,  but  is  only  an  approach,  it  is  not 
the  sound.  The  friction  of  pleurisy  resembles  it  in  tone, 
and  is  very  apt  to  be  produced  in  waves,  the  inspiration 
being  attended  by  an  intermittent  sound  made  by  two  or 
three  ceasings  and  renewals  of  sound.  This  is  not  often 
heard  in  pericarditis.  If  it  is  noticed  its  diagnostic  value 
will  be  appreciated,  as  it  does  not  occur  in  endocardial 
murmurs. 

In  1850,  or  thereabouts,  I  was  able  to  add  a  fact  in  aid 
of  this  distinction,  which  has  since  been  announced  annu- 
ally in  my  lectures,  but  so  far  as  I  remember  has  not 
appeared  in  print.  I  should  say,  so  far  as  I  know,  for 
many  of  my  lectures  have  been  reported  for  medical  jour- 
nals which  I  do  not  habitually  read.  The  lecture  is 
oftener  taken  without  permission  than  with  it,  and  after 
it  is  printed  neither  the  reporter  or  the  editor  has  the 
grace  to  send  me  a  copy  of  the  journal.  I  often  learn  the 
fact  from  physicians  who  make  by  letter  or  otherwise 
inquiries  about  ideas  that  I  did  not  know  had  appeared 
in  print.     The  fact  to  which  I  refer  is  this : 

At  the  time  already  referred  to  I  was  examining  a 
woman  who  had  just  been  admitted  to  hospital.  She  had 
pneumonia  and  pericarditis.  (I  had  by  that  time  learned 
to  search  for  pericarditis  when  I  found  pneumonia.)  In 
listening  to  the  heart  sounds,  it  struck  me  that  I  heard 
the  friction  most  distinctly  on  the  turn  of  the  respiration 
from  inspiration  to  expiration.  I  listened  till  I  was 
assured  that  this  was  a  fact,  then  requested  those  who 
were  with  me  to  verify  it,  while  I  reflected  on  it.  The 
thought  was,  why  not?     In  inspiration  the  ribs  are  lifted 


50  PERICARDITIS. 

Up,  and  their  pressure  on  the  heart  is  at  the  minimum. 
The  moment  the  inspiration  ceases  the  rib  begins  to 
descend,  and  consequently  make  some  pressure  on  the 
heart.  This  would  make  the  contact  of  pericardium  and 
heart  more  close.  But  if  this  is  the  cause  of  the  louder 
sound,  all  the  more  will  it  be  increased  when  the  patient 
takes  a  deep  breath  and  holds  it  while  we  listen.  I  imme- 
diately tried  this  method  on  this  patient.  It  required 
only  a  minute  to  ascertain  that  each  time  the  breath  was 
held  in  this  manner  the  sound  was  increased  in  quantity. 
We  corroborated  this  observation  day  by  day,  so  long  as 
the  friction  sound  remained  in  this  patient. 

The  next  person  to  whom  I  could  apply  this  method 
was  the  son  of  one  of  my  colleagues.  He  had  pericarditis 
without  pneumonia,  and  I  was  disappointed  to  find  that 
when  he  filled  his  chest  and  then  stopped  breathing  the 
friction  sound  was  not  only  not  increased  but  was  actually 
diminished.  What  now  becomes  of  my  little  discovery? 
Was  it  no  discovery,  or  was  there  something  in  this 
patient  in  which  his  make-up  differed  from  that  of  the 
first  ?  I  had  him  take  a  long  breath  and  hold  it  while  I 
percussed  over  the  heart.  There  was  an  unusual  amount 
of  'resonance.  From  this  it  appeared  that  the  fully  ex- 
panded lungs  overlapped  the  heart,  and  that  a  half  breath 
held  in  the  same  manner  might  give  a  different  result.  I 
tried  it  and  got  the  same  increase  as  in  the  first  case. 
When  the  breath  is  held  in  any  condition  of  inspiration 
or  expiration,  the  pressure  of  the  walls  of  the  chest  on  its 
contents  is  increased. 

Further  study  in  this  direction  taught  me  that  endocar- 
dial sounds  are  not  increased  by  a  full  inspiration  held, 
but  if  modified  at  all  they  are  diminished. 

These  observations  were  made  between  thirty  and  forty 
years  ago.  The  rules  drawn  from  them  have  been  an- 
nounced  to   medical   classes    annually   since   that  time. 


PERICARDITIS.  5 1 

They  are,  to  me  at  least,  the  easiest  and  most  rapid 
means  of  distinguishing  pericarditis  when  there  is  a  fric- 
tion sound.  But  if  there  is  none?  In  the  greater  number 
of  cases  the  physician  will  find  it  at  his  first  visit.  After 
a  day  or  two  it  will  disappear,  and  after  five  to  seven 
days  more  it  can  be  heard  again.  On  its  reappearance  it 
has  but  a  short  duration — one  or  two  days.  The  explan- 
ation of  these  physical  changes  is  very  simple.  Early  in 
the  inflammation  there  is  exudation  of  fibrine  and  the 
pericardium  is  in  contact  with  the  heart.  Hence  the 
friction.  By  the  third  or  fourth  day  the  pericardium  is 
lifted  off  the  heart  by  serous  exudation,  and  anteriorly, 
at  least,  there  is  no  contact — no  friction.  After  a  time, 
five  or  six  days,  the  inflammation  has  so  far  abated  that 
the  serum  is  in  great  degree  absorbed  and  there  is  again 
more  or  less  contact  of  the  pericardium  and  heart.  Both 
surfaces  are  rough  and  the  friction  is  renewed  with  its 
proper  sound.  This  renewal  is  heard  first  in  systole,  and 
then  both  systole  and  diastole.  In  other  words,  it  becomes 
double  in  the  same  manner  as  the  first  friction  sound 
does.  But  this  return  sound  soon  ceases  in  diastole  first, 
and  then  in  systole,  because  of  the  coalescence  of  the  per- 
icardium and  heart.  Thereafter  there  can  be  no  more 
friction  sound  till  these  parts  are  separated  one  from  the 
other  in  the  manner  already  described.  Regarding  the 
first  friction  sound,  I  said  just  now  that  when  the  serous 
effusion  lifts  the  pericardium  off  the  heart  the  friction 
ceases,  at  least  on  the  front  of  the  chest.  I  had  in  mind 
at  that  moment  a  medical  student  who  attended  lectures 
for  several  days  after  he  was  attacked  by  pericarditis.  He 
did  not  feel  well,  to  be  sure,  but  his  chief  complaint  was 
of  dyspnoea  in  mounting  the  stairs.  I  examined  him 
while  standing  erect  and  while  lying  down.  I  found  a 
large  region  of  dulness  on  percussion,  but  no  friction 
sound  ;  but  placing  him  on  two  chairs  on  his  back,  so  that 


52  PERICARDITIS. 

I,  sitting  on  the  floor,  could  apply  my  ear  to  the  inferior 
end  of  the  scapula,  I  then  heard  the  friction  distinctly 
enough.  Turning  on  the  same  two  chairs  so  that  I  could 
from  below  upward  place  my  ear  on  the  cardiac  region,  I 
again  heard  it.  In  other  words,  the  specific  gravity  of 
the  heart  is  higher  than  that  of  the  fluid  which  bathes  it, 
and  it  sinks  to  the  most  dependent  part  of  the  sac. 
The  flexible  stethoscope  is  convenient  for  such  an  ex- 
amination. 

An  acute  serous  exudation  into  the  pericardium,  in  the 
absence  of  dropsy  of  other  parts,  is  about  as  sure  a  sign 
of  pericarditis  as  the  friction.  It  is  important,  therefore, 
to  know  how  to  recognize  it.  A  friction  sound  recognized 
and  ceasing  after  two  or  three  days  can  hardly  be  made 
silent  by  anything  except  serous,  or  purulent  or  sero- 
purulent  fluid.  Here,  then,  is  the  first  evidence  of  its 
presence  in  pericarditis.  I  have  already  given  the  dimen- 
sions of  the  heart  and  the  points  on  the  chest  which  cor- 
respond with  its  boundaries.  Now,  if  the  region  of  dul- 
ness  exceeds  these  limits  in  any  noticeable  degree  it  is 
caused  by  hypertrophy  of  the  heart,  or  by  dilatation,  or 
by  morbid  growth  on  the  organ,  or  by  fluid  in  the  peri- 
cardium. If  the  disease  is  acute  and  the  region  of  dul- 
ness  grows  day  by  day,  it  is  fluid  effusion.  Ascertaining 
the  extended  dulness,  you  may,  as  I  have  already  sug- 
gested, learn  by  auscultatory  percussion  how  much  of  it 
is  made  by  the  heart  and  how  much  by  something  else. 
Observe  in  this  specimen  the  relations  of  pericardium  and 
the  great  vessels.  The  serous  pericardium  of  the  heart 
ascends  on  the  anterior  face  of  the  aorta  an  inch  or  more 
before  it  is  reflected  off  on  the  inner  surface  of  the  fibrous 
pericardium.  In  other  words,  the  pericardial  cavity  ex- 
tends upward  above  the  base  of  the  heart  an  inch  or 
more.  This  extension  upward,  however,  is  confined  to 
the  anterior  face  of  the  organ,  and  the  space  given  to  it 


PERICARDITIS.  ^3 

is  only  about  one  and  a  half  inches  wide.  Yet  this  lim- 
ited extension  of  the  cavity,  perhaps,  I  may  say,  may  give 
you  unexpected  assistance  in  your  search  after  serous 
effusion.  The  heart,  as  I  have  just  told  you,  is  heavier 
than  the  fluid  of  the  pericardium.  The  fluid,  therefore, 
will  not  displace  the  heart,  but  will  rise  above  it  and  fill 
the  portion  of  the  cavity  just  described  before  it  distends 
the  pericardium  laterally.  ■  The  base  of  the  heart  is  fixed 
at  the  line  of  the  third  rib,  and  bound  as  it  is  by  vessels 
given  off  upward  and  by  others  coming  into  it  from  above 
and  from  below,  no  ordinary  power  will  move  it.  For  pres- 
ent purposes  you  may  assume  that  as  immovable.  A  dul- 
ness  occurring  above  the  third,  extending  to  the  second, 
will  signify  fluid  effusion,  and  as  it  gradually  but  pretty 
rapidly  extends  the  heart  bag  to  the  left  and  to  the  right, 
you  cannot  doubt  that  you  have  to  do  with  pericarditis. 
But  there  are  other  means  of  diagnosis. 

The  enlarging  heart  sac  will  of  course  push. the  lung  to 
the  right  and  to  the  left  of  its  natural  position,  and  this 
will  diminish  the  amount  of  respiratory  sound  heard  over 
the  proper  pericardium,  so  that  it  will  appear  to  be  dis- 
tant or  be  inaudible.  Next,  then,  will  be  enlargement  or 
fulness  of  the  pericardium  in  proportion  to  the  quantity 
of  fluid  effusion.  In  young  persons  this  will  be  most  evi- 
dent. It  is  in  them  that  the  "  pear-shaped  "  swelling  is 
most  often  seen.  This  swelling  has  its  neck  upward, 
formed  in  that  portion  of  the  sac  that  extends  above  the 
third  rib,  and  base  downward  on  the  diaphragm  and  to  the 
left.  In  persons  of  mature  age  this  **  tumor"  may  be  no 
more  than  a  visible  fulness  of  the  front  on  the  left  side,  a 
convexity  rather  than  concavity  of  the  intercostal  tissues. 
This  difference  is  referred  to  the  yielding  nature  of  the 
ribs  in  young  persons  and  their  firmer  character  as  age 
advances. 

The  quantity  of  serous  effusion  that  may  occur  in  peri- 


54  PERICARDITIS. 

carditis  is  set  down  as  three  pints  and  more  ;  when  the  quan- 
tity is  very  large  another  thing  may  occur.  I  was  many 
years  ago,  requested  to  visit  a  patient  half  a  day's  journey 
up  the  river.  I  could  not  go  on  the  day  the  application  was 
made,  and  requested  a  young  physician,  who  had  lately 
gone  through  a  hospital  service  with  great  credit  and  in 
whose  skill  and  accuracy  in  the  interpretation  of  the 
physical  signs  I  had  full  confidence.  When  he  returned 
he  informed  me  that  the  lady  had  pneumonia  of  the  left 
lung.  I  visited  her  the  next  day  and  found  bronchial 
breathing  and  bronchial  voice  enough  for  the  worst  of 
pneumonias,  on  the  left  side  behind,  but  no  breath  sound 
of  any  kind  could  be  heard  on  the  left  front.  The  patient 
had  had  no  chill,  no  rusty  expectoration,  and  the  dulness 
could  be  followed  from  the  place  in  front  where  there  was 
no  respiratory  sound  to  the  line  where  the  bronchial  breath- 
ing became  distinct ;  from  that  to  the  spine  the  dulness  was 
marked,  but  less  than  up  to  that  line.  Then  there  was 
prominence  of  the  pericardial  space  and  dulness  extending 
upward  to  second  rib  and  under  it.  In  short,  it  was  a  case 
of  pericarditis  with  large  pericardial  fluid  effusion,  and  not 
one  of  pneumonia.  This  gentleman  was  then  skilful  and 
has  risen  to  great  distinction.  He  could  have  made  the 
diagnosis,  but  the  signs  of  pneumonia  so  impressed  him 
that  he  shut  himself  off  from  the  other  possibilities.  A 
full  inquiry  into  other  conditions  that  could  produce 
these  signs  would  have  set  him  right.  I  have  said  that 
the  rational  symptoms  of  pericarditis  are  in  the  main  of 
little  worth,  but  such  a  case  as  this  is  an  exception.  In 
this  lady  the  distress  for  breath  was  pitiful ;  she  could 
not  sleep  in  the  recumbent  position ;  only  in  a  chair. 
She  could  not  bear  the  weight  of  this  sac  of  water  on  her 
lung,  in  addition  to  the  displacement  caused  by  its  bulk. 
I  have  already  narrated  one  case  which  shows  how  the 
bodily  strength  may  be  maintained  while  pericarditis  is 


PERICARDITIS.  55 

making  its  invasion.  Another  may  be  instructive.  A 
young  gentleman,  a  lawyer  by  profession,  left  his  home 
in  Vermont  with  the  intention  of  transacting  business  in 
several  cities  When  he  reached  Troy  he  felt  ill ;  he  could 
hardly  say  how,  but  his  breathing  and  pulse  were  rriore  fre- 
quent than  usual.  He  sent  for  a  physician,  who  told  him 
that  he  had  pericarditis,  and  bled  him  and  also  advised  him 
to  return  to  his  home.  This,  advice  he  did  not  accept,  but 
the  next  morning  went  on  his  journey.  I  saw  him  in  New 
York  and  found  that  the  opinion  given  in  Troy  was  correct 
and  that  he  had  already  considerable  fluid  in  the  pericar- 
dium. I  advised  him  not  to  go  home,  but  to  go  to  bed. 
This  advice  he  would  not  follow,  but  persevered  in  the 
transaction  of  his  business.  He  spent  three  or  four  days 
in  New  York,  went  to  Philadelphia  and  Boston,  and 
reached  his  home  fourteen  days  after  his  disease  was  diag- 
nosticated in  Troy,  all  the  time  engaged  in  business. 

There  are  a  few  cases  of  pericarditis  that  run  their  course 
so  quietly,  with  so  little  local  and  general  disturbance, 
that  nothing  is  known  of  it  till  the  evidences  are  revealed 
after  death — death  having  been  caused  by  some  other 
disease.  From  this  degree  of  mildness  the  symptoms 
vary  all  the  way  up  to  the  distress  and  suffering  observed 
in  the  lady  whose  case  was  just  now  narrated.  Com- 
monly you  Avill  find  the  patient  lying  on  his  back,  his 
breath  twenty-five  or  thirty  in  a  minute ;  the  pulse 
eighty  to  one  hundred  in  the  same  time ;  and  the  tempera- 
tion  100°  or  101° — not  a  great  sufferer,  though  Louis 
and  Valleix  found  actual  pain  oftener^than  I  have,  that  is, 
in^about  half  of  their  cases.  He  keeps  his  bed,  not  because 
he  cannot  walk  about,  but  because  he  is  more  comfortable 
in  it.  Bouillaud  at  one  time  attached  importance  to  a 
noise  in  the  heart  beat  which  can  be  imitated  by  placing 
the  palm  of  the  hand  over  the  ear  and  percussing  the  back 
of  it  by  a  quick  blow  from  one  finger  of  the  other  hand. 


56  PERICARDITIS. 

But  when  it  was  found  that  a  heart  made  irritable  by  any 
cause  gave  the  same  sound,  its  diagnostic  importance  was 
greatly  reduced. 

The  circumstances  under  which  the  rational  symptoms 
are  the  least  diagnostic  are,  probably,  those  observed 
when  pericarditis  is  ingrafted  on  acute  rheumatism.  There 
is  already  fever  and  the  common  symptoms  of  it,  and 
whether  there  is  more  or  less  of  it,  in  these  days  of  aus- 
cultation no  experienced  person  allows  himself  to  be 
guided  by  them  alone  ;  on  the  contrary,  he  pays  little  heed 
to  them  and  forms  his  opinion  from  the  physical  signs. 
This  is  nearly  or  quite  as  true  when  pericarditis  becomes 
a  complication  of  pneumonia. 

The  mortality  of  pericarditis,  uncomplicated,  is  small, 
almost  nothing.  Latham  had  no  death  from  pericarditis 
alone  in  the  cases  already  cited.  Although  he  had  three 
from  pericarditis  and  endocarditis  combined.  When  it 
occurs  in  the  course  of  acute  rheumatism,  the  two  together 
are  rarely  fatal ;  but  when  it  occurs  in  the  oedema  of 
scarlet  fever,  it  is  always  grave  and  often  fatal.  The  same 
is  true  of  its  coincidence  with  granular  kidney.  When  it 
occurs  with  pneumonia  it  is  difficult  to  estimate  its  impor- 
tance, but  it  can  hardly  be  doubted  that  it  makes  some 
cases  of  that  disease  fatal  that  without  it  might  have 
recovered.  Single  pleurisy,  not  reaching  empyema,  is  very 
rarely  fatal,  and  it  does  not  seem  that  coincident  peri- 
carditis adds  to  it  a  fatal  weight. 

When  pericarditis  is  secondary,  it  is  a  question  of  some 
interest,  at  what  stage  of  the  primary  affection  is  it  devel- 
oped ?  In  the  oedema  of  scarlet  fever,  if  it  occurs  at  all,  it 
maybe  looked  for  in  seven  to  ten  days  from  the  beginning 
of  the  swelling.  It  may  come  later,  but  the  danger  of  this 
complication  diminishes  daily  after  ten  days.  With  the 
granular  kidney  it  has  no  fixed  time.  In  a  very  large  pro- 
portion of  the  cases  of  this  disease  it  does  not  occur  at  any 


PERICARDITIS.  57 

time,  and  when  it  occurs  the  event  is  associated  with 
scanty  and  high  colored  urine  and  an  imperfect  separation 
of  the  urea  from  the  blood.  In  other  words,  althou^di  it  is 
not  often  found  in  those  who  die  of  the  convulsions  so 
frequent  in  the  advanced  stage  of  this  affection,  still  the 
same  condition  of  the  kidneys  seems  to  be  associated  with 
both,  and  this  condition  is  often  induced  by  imperfect  pro- 
tection from  the  cold,  or  the  use  of  alcoholic  liquors. 
Therefore,  to  know  when  there  is  danger  of  pericarditis  in 
granular  kidney  we  must  know  when  the  patient  is  going  to 
be  imprudent.  It  is  not  often  in  the  first  year,  but  when 
after  two  or  three  years  the  patient,  finding  himself  still 
alive  and  comfortable,  begins  to  doubt  his  danger  and 
become  impatient  of  advice. 

In  pneumonia  it  is  only  in  exceptional  cases  that  peri- 
carditis occurs,  and  nobody  has  attempted  to  fix  the  day 
of  its  occurrence.  I  have  only  very  rarely  seen  the  concur- 
rence in  private  practice.  It  is  in  the  hospital  that  I  have 
become  acquainted  with  it  chiefly.  Persons  attacked  by 
pneumonia  do  not  often  get  into  the  hospital  before  the 
third  day  of  their  disease.  In  no  instance  that  I  can  recall 
was  the  pericarditis  developed  after  admission,  but  in  all 
cases  it  was  found  in  the  first  examination  of  the  patient. 
This  is  equivalent  to  saying,  as  far  as  a  limited  experience 
can  say  anything,  that  it  belongs  to  the  first  three  or  four 
days  of  pneumonia,  but  it  does  not  inform  us  whether  the 
two  diseases  arise  from  one  diathesis  and  are  contempera- 
neous  in  their  attack,  or  whether  the  pericarditis  is  second- 
ary. You  have  been  informed  that  albumen  appears  in 
the  urine  of  all  cases  of  severe  pneumonia  early,  at  least 
as  soon  as  there  is  consolidation,  and  that  in  its  course 
symptoms  of  uraemic  poisoning  are  not  uncommon.  It  is 
possible  that  this  pericarditis  is  caused  by  this  same 
poison.  Whether  it  is  or  not  is  still  a  problem  to  be 
solved. 


58  PERICARDITIS. 

In  the  few  cases  of  concurrent  pleurisy  and  pericarditis 
writers  are  commonly  satisfied  with  assuming  that  the 
inflammation  extends  from  one  membrane  to  the  other, 
and  they  do  not  state  from  observation  which  is  primary, 
but  leave  us  the  inference  that  the  pleuritic  inflammation 
extends  to  the  pericardium.  If  this  is  really  the  fact,  then 
we  may  turn  to  it  for  an  explanation  of  the  concurrence 
of  pneumonia  and  pericarditis,  for  it  is  very  rare  that 
pneumonia  is  not  a  pleuro-pneumonia,  and  the  J^osit  niortein 
evidences  of  pleurisy  are  often  more  marked  than  they 
are  in  simple  pleurisy.  But  if  the  extension  theory  be 
correct,  why  is  it  so  rarely  illustrated  ?  for  there  are  hun- 
dreds of  cases  of  either  without  any  sign  of  inflammation 
in  the  other.  Indeed,  I  think  I  may  say  they  do  not 
concur  once  in  fifty,  perhaps  a  hundred  times.  I  do  not 
remember  that  I  have  ever  seen  it,  and  therefore  have  no 
faith  of  my  own  to  state. 

Regarding  rheumatic  pericarditis,  however,  I  .  am  on 
very  different  ground  ;  with  this  I  am  familiar.  While  it 
is  true  that  the  rheumatic  diathesis  is  in  rare  instances 
declared  by  pericarditis  before  the  pains  appear  in  the 
joints,  and  these  do  actually  follow  after  some  days ;  the 
great  rule  is  that  the  articular  rheumatism  precedes  the  car- 
diac affection.  Such  an  exception  was  reported  by  my  pre- 
decessor in  this  chair.  I  have  witnessed  two  or  three  cases, 
and  a  case  is  recorded  now  and  then  by  writers.  These 
cases,  then,  are  so  rare  that  they  deserve  little  more  atten- 
tion than  the  announcement  of  the  possibility ;  especially 
as  there  is  nothing  in  them  to  inform  us  of  their  rheumatic 
origin,  nothing  to  suggest  a  treatment  of  rheumatism,  any 
serous  membrane  may  become  inflamed  in  the  course  of 
rheumatism,  but  the  pericardial  serous  membrane  is  at- 
tacked ten  or  twenty  times  more  frequently  than  any  other. 
This  is,  perhaps,  accounted  for  by  the  fact  that  articular- 
rheumatism  is  an  inflammation  of  the  fibrous  tissues  of  the 


PERICARDITIS.  59 

joints,  and  that  this  membrane  is  the  only  one  that  is  in 
contact  with  and  attached  to  a  pretty  firm  fibrous 
structure — the  fibrous  pericardium.  This  is  not  identical 
in  tissue  with  that  of  ligaments  of  the  joints,  but  there  is 
a  resemblance  between  them  nearer  than  between  any 
other  two  tissues  of  the  body.  This  suggests  the  idea 
that  the  fibrous  pericardium  may  attract  rheumatism  as 
fibrous  structures  of  joints,  but  less  strongly,  and  transmit 
it  directly  to  its  serous  lining.  The  time  when  this  com- 
plication occurs  is  not  commonly  till  the  fifth  day  after 
the  joints  are  attacked.  From  this  to  the  eleventh  day 
the  liability  is  greatest.  This,  in  my  view,  is  an  impor- 
tant fact.  For  if  rheumatic  pericarditis  delays  till  the 
fifth  day  of  the  articular  disease,  and  if  we  can  cure  the 
latter  in  less  than  five  days,  can  we  not  save  hundreds  of 
hearts?  Since  the  salicylate  of  soda  has  been  relied  on 
for  cure  of  rheumatism,  many  cases  are  cured  in  one  day 
and  few  persist  till  the  fifth.  That  is,  the  inflammation 
is  subdued,  but  stifl^ness  remains  for  a  day  or  two  more. 
I  think  I  have  seen  many  instances  of  this  protection  of 
the  heart.  Of  European  writers  some  admit  this  ;  others 
deny  it.  To  my  mind,  this  difference  arises  from  the  fact 
that  they  do  not  all  use  the  drug  in  the  same  way,  and 
in  the  same  doses. 

Treatment  of  Pericarditis. — As  late  as  1840  the  treat- 
ment of  pericarditis  without  a  mercurial  was  generally  re- 
garded as  hardly  less  than  malpractice,  and  it  was  to  be 
carried  to  the  production  of  redness  of  the  gums  and  slight 
salivation.  Dr.  Latham,  whose  pleasing  style  won  for 
his  book  a  world  of  readers,  knew  no  other  way,  and 
urged  his  views  with  great  earnestness.  The  idea  was 
that  the  mercurial  ''  diminished  the  plasticity  of  the 
blood"  and  prevented  the  plastic  effusion,  and  thus  gave 
the  patient  a  better  chance  of  recovery.  Soon  after  the 
publication  of  this  pleasing  book   Dr.  Taylor  published 


6o  PERICARDITIS. 

the  results  of  a  different  treatment  in  another  hospital. 
He  gave  no  mercurial  whatever,  and  his  results  in,  it  may 
be,  fifty  cases  were  as  good  and,  as  I  remember,  better 
than  those  of  Dr.  Latham.  This  greatly  surprised  the 
advocates  of  that  treatment,  and  was  the  beginning  of  its 
abandonment,  as  a  plan.  Now  a  physician,  who  has 
charge  of  a  case  of  pericarditis  hardly  thinks  of  a  mercu- 
rial of  any  kind,  and  it  is  not  given  in  one  case  out  of 
twenty. 

The  first  consideration,  as  the  disease  is  so  often 
secondary,  is  the  treatment  proper  for  the  primary  affec- 
tion. If,  for  example,  it  follows  articular  rheumatism, 
the  question  will  be,  what  will  most  quickly  and  safely 
eradicate  the  rheumatic  diathesis?  This  leads  to  some 
statements  regarding  the  treatment  of  articular  rheuma- 
tism. Until  Dr.  Fuller's  alkaline  treatment  was  an- 
nounced we  were  much  at  sea ;  hardly  two  physicians 
agreed  on  any  plan.  One  relied  on  nitre,  in  large  doses, 
and  greatly  diluted.  Another  thought  that  lemon-juice, 
given  freely,  gave  him  better  results.  Another  gave 
quinine.  A  fourth  relied  chiefly  on  diaphoretics,  and  still 
another  had  faith  in  the  external  application  of  boiled 
boughs  used  as  hot  as  could  be  borne.  But  treated  by 
whatever  plan  it  was  but  slowly  cured,  if  cured  at  all.  It 
often  lingered  for  two  and  three  months.  But  the  adop- 
tion of  Dr.  Fuller's  plan  was  attended  by  a  notable  short- 
ening in  the  duration  of  the  disease,  which  was  cured  in 
three  to  six  days  in  a  large  proportion  of  the  cases.  A 
few  resisted,  and  the  disease  was  not  controlled  for  weeks. 
The  plan  had  memorable  advantages  over  any  previously 
proposed,  and  was  in  detail  this,  or  rather  is  this:  the  ad- 
ministration of  an  alkaline  medicine  in  full  doses  so  as  to 
make  the  urine  alkaline  in  the  shortest  time  consistent  with 
the  toleration  of  the  stomach.  He  used  sometimes  the 
Rochelle  salt,  tartrate  of  potash  and  soda ;  sometimes  the 


PERICARDITIS.  6l 

carbonate  or  bicarbonate  of  soda  ;  sometimes  the  same 
salts  of  potash.  He  had  the  urine  tested  at  short  inter 
vals  to  ascertain  when  this  saturation  had  occurred.  After 
such  saturation  the  urine  was  to  be  kept  alkaline  till  the 
symptoms  abated,  requiring,  usually,  smaller  doses  than 
were  needed  to  produce  the  alkalinity.  This  is  the  pith 
of  the  matter. 

About  ten  years  ago  the:  salicylic  acid  was  introduced 
for  the  cure  of  rheumatism,  and  the  physicians  of  Bellevue 
Hospital,  prominently  Dr.  Jacobi,  desired  to  try  it  ;  but 
how  to  dissolve  it  was  the  question.  He  proposed  the 
carbonate  or  bicarbonate  of  soda  as  the  solvent.  The 
acid  was  mixed  with  water  first,  and  then  the  soda  was 
added  till  the  mixture  became  clear.  This  was  the  first 
salicylate  of  soda  made  in  this  country,  so  far  as  I  know, 
and  with  it  the  disease  was  treated  with  marked  success. 
I  published  a  dozen  cases,  or  so,  soon  after  this  prepara- 
tion came  into  use,  showing  the  almost  marvellous  prompt- 
ness with  which  this  medicine  gave  relief.  I  can  narrate 
some  others,  indeed  many,  but  will  not  be  wearisome. 

A  man,  of  about  middle  age,  was  brought  into  one  of 
my  wards  when  I  was  present.  I  found  his  right  knee 
swollen,  red,  hot,  and  painful,  so  that  he  could  not  move 
it.  The  disease  had  been  upon  him  two  days.  He  had 
some  fever.  Salicylate  of  soda  was  prescribed,  twenty 
grains  in  solution  every  two  hours.  No  other  medicine 
was  given.  The  next  day  at  the  same  hour  the  swelling, 
redness,  and  pain  were  gone;  only  stiffness  remained. 
The  medicine  was  continued,  but  diminished  to  half  the 
quantity.  The  next  day  I  found  him  sitting  up  and  he 
could  walk.  On  the  third  day  he  asked  for  his  discharge, 
and  was  discharged.     I  heard  no  more  of  him. 

A  young  lady  of  remarkably  handsome  figure  and  face, 
before  I  knew  her,  had  had  three  several  attacks  of  rheuma- 
tism from  one  to  two  years  apart.     She  had  been  confined 


62  PERICARDITIS. 

to  her  bed,  or  arm-chair,  by  each  invasion,  an  average  of 
three  months,  and  in  each  the  heart  had  suffered.  She 
came  with  her  mother  to  the  city  for  a  stay  of  a  few 
days.  Her  mother  had  previously,  and  again  at  this 
visit  to  the  city,  consulted  me  regarding  her  own  ailments. 
One  morning  she  came  to  me  with  a  very  sad  face,  and 
told  me  that  her  daughter,  since  the  day  before,  had  been 
brought  to  bed  with  a  new  attack  of  rheumatism,  which 
appeared  to  be  the  worst  she  had  ever  had.  Both  knees, 
both  elbows,  and  one  ankle  were  red,  painful,  and  swollen, 
and  that  she  was  utterly  helpless,  "and  now,"  she  said, 
*'  my  poor  child  must  suffer  another  three  months  of 
agony,"  and  she  wept.  I  bade  her  be  comforted,  told 
her  that  the  world  moves  and  men  make  discoveries,  that 
*'  the  thing  that  hath  been,  is"  not  now,  always,  "  the 
thing  that  shall  be,"  and  that  by  the  use  of  a  new  medi- 
cine, I  hoped  to  give  her  daughter  pretty  prompt  relief. 
It  was  ten  o'clock  in  the  morning.  I  prescribed  the  salicy- 
licate  of  soda,  fifteen  grains  every  two  hours.  I  could 
not  visit  her  till  nine  o'clock  at  night.  I  was  happy  to 
find  her  almost  wholly  reheved  of  pain,  and  the  mother 
informed  me  that  the  swelling  and  redness  were  diminish- 
ing. She  rested  well  that  night.  The  next  day  at  i  P.M., 
I  found  her  sitting  in  a  chair  at  the  side  of  her  bed  free  from 
all  the  symptoms  of  rheumatism  except  stiffness  in  the 
invaded  joints.  The  third  day  she  could  walk.  Thus 
ended  her  rheumatism,  and  thus  was  lifted  from  her 
mother's  heart  a  load  of  sorrow.  That  was  the  end.  I 
saw  her  three  years  later.  Her  old  heart  disease  remained, 
but  there  had  been  no  more  rheumatism. 

These  are  selected  cases,  and  selected  for  the  purpose 
of  showing  with  what  energy  and  promptness  the  medi- 
cine acts  in  certain  cases ;  and  especially  to  show  that  the 
drug  can,  in  many  cases,  at  least,  strangulate  a  rheuma- 


PERICARDITIS.  63 

tism  before  the  average  period  arrives  for  the  occurrence 
of  heart  complications. 

There  exists  in  my  mind  no  doubt  that  the  promptest, 
best,  and  safest  remedy  for  articular  rheumatism,  and 
consequently  the  best  prevention  of  its  secondary  cardiac 
disease,  is  the  salicylate  of  soda.  Still  there  are  certain 
facts  which  should  be  stated  per  contra.  Given  in  the 
quantity  just  reported  it  does,  in  some  persons,  either  by 
its  direct  action  on  the  stomach,  or  through  the  nervous 
system,  produce  vomiting  ;  then  it  is  given  in  smaller 
doses,  or  it  is  suspended  for  a  few  hours,  and  the  bicar- 
bonate of  soda  given  instead. 

Early  in  the  use  of  the  salicylate  of  soda,  it  was  noticed 
that  now  and  then  delirium  followed  its  administration,  and 
seemed  to  be  produced  by  it.  This  effect  seemed  to  be 
chiefly  observed  in  persons  who  had  abused  themselves 
by  too  free  a  use  of  intoxicating  liquors.  This  delirium 
occurred  almost  exclusively  in  hospital  patients,  whose 
"  previous  history"  it  is  often  impossible  to  get.  The  de- 
lirium is  violent,  yet  it  was  commonly  thought  prudent 
to  send  these  patients  to  the  wards  where  the  delirious 
are  treated.  This  mental  disorder  lasted  but  a  day  or 
two,  and  has  been,  in  no  case,  followed  by  any  permanent 
disease.  In  these,  again,  the  carbonate  or  bicarbonate 
was  given  instead  of  the  salicylate. 

The  salicylic  acid  has  been  given  alone.  It  will  cure 
articular  rheumatism,  but  less  promptly,  it  appears  to  me, 
than  the  salt.  The  European  reputation  of  the  acid  led 
Dr.  Jacobi,  almost  without  knowing  it,  to  make  and  use 
the  salicylate,  and,  for  myself,  I  must  say  that  after  sev- 
eral years  use  of  it,  it  has,  at  present,  my  decided  prefer- 
ence. 

The  abstraction  of  blood  is  hardly  ever  thought  of  in 
the  treatment  of  articular  rheumatism,  so  it  is  almost 
never  resorted  to  for  the  cure  of  rheumatic  pericariditis 


64  PERICARDITIS. 

The  aim  is  to  overcome  the  rheumatic  diathesis  and  so 
cure  both. 

When  pericarditis  occurs  in  the  oedema  after  scarlet 
fever,  it  is  probably  produced  by  uraemia,  or  the  same 
condition  of  the  system  that  causes  the  dropsy,  and  is 
almost  always  attended  by  a  high-colored,  or  bloody,  or 
smoky  and  scanty  urine.  The  first  object  of  treatment, 
then,  is  to  remove  the  cause  of  the  disease  ;  in  other 
words,  to  induce  a  healthy  secretion  of  urine,  if  that  is 
possible,  and  remove  from  the  system  the  poison  that  is 
being  carried  into  every  part  of  it,  whether  that  poison 
be  urea,  carbonate  of  ammonia,  or  whatever  else.  To 
accomplish  this  the  most  valuable  agents  are  the  diuretics 
and  diaphoretics.  Among  the  first,  I  give  preference  to 
an  extemporaneous  citrate  of  potash  and  digitalis.  You 
prescribe  half  an  ounce  of  the  carbonate  of  potass,  dis- 
solved in  six  ounces  of  water,  and  direct  that  a  tablespoon- 
ful,  mixed  with  the  same  quantity  of  fresh  lemon-juice, 
be  given  every  two  hours,  to  an  adult,  with  the  proper 
reduction  for  children.  On  the  mixture  of  these  two  in- 
gredients there  is  a  feeble  effervescence,  but  enough  to 
make  the  draught  agreeable  to  the  taste.  It  is  not  a 
new  prescription.  The  physicians  who  were  old  when  I 
was  young  gave  it  greatly  more  than  does  the  present 
generation.  With  this  give  an  adult  a  dessert-spoonful 
of  the  ififusion  of  digitalis  three  times  a  day.  I  empha- 
size the  word  infusion,  because  it  seems  to  me  to  act 
much  better,  as  a  diruetic,  than  the  tincture,  or  extract,  or 
powder,  and  because  many  physicians  have  thanked  me 
for  the  suggestion.  The  quantity  of  the  infusion  may  be 
larger  than  a  dessert-spoonful.  The  authorized  dose  is  a 
tablespoonful,  but  the  smaller  portion  has  in  most  cases 
been  enough ;  and  then,  the  only  cases  in  which  I  have 
seen  what  are  called  the  '*  cumulative  effects"  of  digitalis 
were  in  uraemic  persons,  and  I  am  afraid  to  give  it  freely 


PERICARDITIS.  65 

to  such  persons.  These  two  medicines  act  better  when 
given  in  this  way  than  when  either  is  given  separately. 
The  potash  salt,  probably,  causes  an  increase  of  water  of 
the  urine,  and  the  digitalis  the  solid,  or  solidifiable  ele- 
ments. 

Everybody  knows  the  relations  that  exist  between  the 
skin  and  kidneys,  and  you  will,  therefore,  be  prepared  to 
hear  that  when  those  organs  are  congested  a  certain 
treatment  of  the  skin  may  help  to  bring  relief.  What  I 
am  about  to  advise  is  more  preventive  than  curative  and  is, 
therefore,  all  the  more  valuable.  As  soon  as  the  oedema 
and  paleness  appear,  use  the  warm  water  or  vapor  bath 
until  a  perspiration  is  produced.  At  first  the  perspiration 
may  be  a  little  free.  In  this  condition  put  the  patient  in 
bed  without  losing  much  time  in  wiping  off  the  water. 
Keep  up  the  sweating  for  half  an  hour,  then  let  it  dry 
down  to  a  mere  moisture,  and  keep  the  patient  in  this 
moisture  for  days,  even  for  two  or  three  weeks,  by  the 
bed-clothes.  In  many  cases  of  children  it  is  almost  impos- 
sible to  keep  the  patient  in  bed.  He  does  not  feel  sick 
and  cannot  understand  why  he  should  not  be  allowed  to 
run  about  as  usual.  In  such  cases  I  have  adopted  the 
plan  of  getting  the  first  perspiration  and  keeping  the  child 
in  bed  for  a  few  hours.  Meantime  a  double  suit  of  flan- 
nel is  prepared — pretty  heavy  flannel — and  when  he  will 
not  tolerate  the  bed  any  longer  he  is  clothed  in  this  suit 
and  allowed  to  walk  about  and  enjoy  his  playthings ;  but 
with  this  one  important  condition,  that  the  temperature  of 
the  room  or  rooms  into  which  he  is  allowed  to  go  be  kept 
at  or  above  'j^f'  F.  This  temperature,  this  clothing,  and 
the  exercise  he  will  get  will  be  likely  to  keep  a  little  sweat 
on  the  forehead  and  body  the  whole  time.  This  is  what  you 
will  try  to  produce  and  keep  up  for  days  together.  You 
may  expect  from  this  management  a  diminution  of  the 
congestion  of  the  kidneys,  and  with  that  a  freer  secretion  of 


66  PERICARDITIS. 

urine,  and  a  gradual  diminution  in  the  morbid  .indications 
of  that  fluid,  and  by  this  the  danger  of  convulsions  and 
pericarditis  is  naturally  reduced.  If  pericarditis  has  actu- 
ally begun,  the  patient  will  probably  remain  in  bed  will- 
ingly, and  the  perspiration  may  be  induced  by  the  foot- 
bath in  bed,  and  kept  up  by  repetition.  The  vessel  hold- 
ing the  warm  water  is  placed  in  bed  close  to  the  body, 
the  thighs  and  knees  so  bent  that  the  feet  will  fall  perpen- 
dicularly into  the  water,  and  all  covered  by  the  bed-clothes. 
This  is  the  first  step  in  the  treatment,  and  may  be  followed 
by  the  depurative  diuretics.  The  condition  of  your  patient 
does  not  suggest  the  lancet,  but  rather  tonics,  including 
iron,  and  if  you  take  any  blood  at  all,  it  should  be  limited 
to  that  which  a  few  leeches  will  abstract.  There  is  prob- 
ably no  therapeutical  fact  more  fully  demonstrated  than 
the  efficacy  of  blisters  in  pleurisy.  Are  they  equally  use- 
ful in  pericarditis  ?  I  do  not  think  so.  In  one  case  the 
blister  is  applied  near,  physiologically,  as  well  as  in  actual 
distance,  to  the  diseased  surface.  In  the  other  the  physi- 
ological distance  is  much  greater.  The  vessels  that  sup- 
ply the  heart  with  blood  have  their  origin  from  the  aorta, 
before  it  leaves  the  heart  sac,  and  the  dependence  of  the 
sac  itself  on  the  thoracic  arteries  is  not  intimate.  A 
blister  applied  over  the  heart  may  act  as  a  derivative  on 
other  branches  of  the  thoracic  vessels,  but  probably  not 
at  all  on  the  coronary  arteries  of  the  heart.  However 
this  may  be,  blisters  are  not  a  favorite  application  in  this 
form  of  pericarditis,  perhaps  because  it  occurs  so  gene- 
rally in  children,  and  the  student  is  admonished  to  use 
them  with  modification  and  great  care  in  these  young 
folks,  on  account  of  the  exaggerated  and  even  dangerous 
effects  they  may  produce. 

Opium  deserves  consideration  in  this  form  of  the  dis- 
ease. It  may  not,  by  any  means,  be  given  in  heroic  doses, 
as  it  is  given  in  the  treatment  of  peritonitis,  for  a  reason 


PERICARDITIS.  67 

which  I  will  soon  explain  to  you  ;  but  given  in  ordinary 
doses,  or  only  slightly  more,  it  soothes  irritation,  and  the 
heart  is  always  irritable  during  the  early  stage  of  peri- 
carditis, and  gives  the  patient  needed  rest,  and  in  this  way 
gives  earlier  development  to  that  recuperation  and  re- 
covery which  in  many  cases  may  be  regarded  as  the 
spontaneous  tendency  of  the  disease  itself.  The  objec- 
tion to  large  doses  of  any  opiate  in  the  course  of  uraemia 
in  any  of  its  manifestations  may  be  enforced  by  the  fol- 
lowing sketches.  The  late  Dr.  Conant  Foster,  living  near 
me,  sent  for  me  early  one  morning  to  see  a  young  man 
who  had  slept  in  his  house.  He  was  comatose,  but  not 
profoundly.  The  history  in  short  was  this  :  He  sought 
the  doctor's  advice  the  night  before  on  account  of  a  great 
pain  in  one  of  his  fingers,  which  was  the  seat  of  a  felon. 
The  doctor  advised  him  to  take  forty  drops  of  laudanum  on 
going  to  bed.  In  the  course  of  the  night  the  patient  sent 
a  message  to  the  doctor,  informing  him  that  the  pain  was 
very  severe  and  he  could  not  sleep.  The  doctor  advised 
him  to  take  another  dose  of  laudanum  of  forty  drops.  In 
the  morning  he  was  found  in  the  state  already  indicated. 
He  could  not  be  aroused  to  answer  questions,  yet  he  was 
not  motionless  in  bed  ;  the  pupils  were  contracted,  but 
not  extremely  ;  he  did  not  swallow  except  unconsciously; 
the  breathing  was  not  remarkably  deep  or  infrequent ;  it 
was  not  the  characteristic  stupor  of  opium-poisoning,  but 
more  hke  that  of  uraemia.  Dr.  Foster  did  not  know  of 
any  illness  before  the  felon  occurred.  There  was  no 
oedema.  The  chance  that  any  laudanum  could  be  found 
in  the  stomach  was  hardly  worth  entertaining,  since  the 
last  dose  was  taken  five  or  six  hours  before,  and  the 
stomach  was  empty  when  it  was  taken.  The  organ  was 
washed  out  by  the  pump,  and  no  odor  of  laudanum  was 
discovered  in  the  water  used.  The  remaining  indication 
was    to    procure    free    perspiration.      I    have    forgotten 


68  PERICARDITIS. 

whether  this  was  done  by  enveloping  the  patient  in  sev- 
eral thicknesses  of  blankets  wrung  out  of  hot  water,  or 
by  use  of  the  foot-bath  in  bed ;  but  our  efforts  were  una- 
vailing. He  died  that  day.  A  post-mortem  examination 
revealed  what  he  and  his  friends  appeared  to  be  wholly 
ignorant  of,  a  rather  advanced  stage  of  Bright's  kidney. 

During  the  week  in  which  I  saw  this  patient  I  was 
called  to  see  a  lady,  in  consultation,  who  showed  evi- 
dences of  Bright's  disease  in  oedema  and  paleness,  mani- 
festly. She  had  the  night  before  taken,  at  one  dose,  half 
a  grain  of  sulphate  of  morphine,  I  do  not  remember  for 
what.  She  was  in  a  coma  similar  to  that  in  which  the 
young  man  was  found,  not  having  the  close  contracted 
pupils,  the  deep  slow  breathing,  the  motionlessness  of  the 
opium  poisoning,  but  again  more  like  that  produced  by 
uraemia  or  the  early  stage  of  miasmatic  coma.  I  have 
seen  other  similar  cases,  enough  to  persuade  me  that 
there  are  conditions,  not  readily  recognized,  in  uraemia, 
in  which  the  blood  poison  and  opium  may  work  together, 
and  produce  a  coma  which  neither  of  them  alone  would 
have  produced,  at  least,  at  the  time  when  it  occurred. 
On  the  other  hand,  many  patients  having  Bright's  disease 
have  taken,  under  my  eye,  but  not  with  my  approval,  half 
a  grain  of  the  sulphate  of  morphine,  night  after  night, 
with  only  soothing  and  sleep-giving  effects.  This  was 
the  case  with  my  colleague,  the  late  Prof.  Oilman.  He 
gave  me  all  the  confidence  I  could  ask,  except  in  this  one 
particular.  I  assented  to  one  quarter  of  a  grain  of  the 
sulphate  at  night,  but  he  would  take,  night  after  night, 
a  half  grain,  to  which  dose  I  gave  my  sanction,  only  after 
the  proof  that  for  him  at  that  time  it  was  not  dangerous. 

These  cases,  it  is  true,  are  neither  of  them  pericarditis, 
but  all  Bright's  disease,  and  if  pericarditis  occurs  with  that 
affection,  either  acute  or  chronic,  they  illustrate  a  needed 
caution  in  its  management. 


PERICARDITIS.  69 

The  co-existence  of  pericarditis  and  pneumonia,  or  of 
pericarditis  and  pleurisy,  is  of  infrequent  occurrence — so 
infrequent  that  it  does  not  suggest  the  thought  that 
one  is  secondary  to  the  other,  as  we  are  apt  to  say 
pericarditis  is  to  rheumatism.  It  seems  to  be  a  con- 
currence, as  if  the  same  diathesis  had  produced  them 
both.  There  would  seem  to  be  then  nothing  distinctive 
in  the  treatment  of  such  a  pericarditis.  What  we  would 
do  for  one  we  would  do  for  the  other.  Then  for  the  treat- 
ment of  pneumonia.  When  I  entered  the  profession 
bleeding  from  the  arm  was  almost  invariable.  The  pa- 
tient was  bled  as  soon  as  the  diagnosis  was  made.  Com- 
monly sixteen  ounces  of  blood  were  taken,  or  the  blood 
was  allowed  to  flow  till  the  patient  sitting  on  his  bed 
grew  pale,  and  the  sweat  bedewed  his  forehead.  In 
twelve  hours  the  same  thing  was  repeated,  and  after  an- 
other interval  of  twelve  hours,  ten  or  twelve  ounces  were 
taken  by  cups  or  leeches.  Bleeding,  more  or  less,  in 
pneumonia  was  so  general  that  its  omission  was  regarded 
as  hardly  less  than  culpable,  and  the  first  implement  with 
which  the  student  supplied  himself  was  a  lancet.  In  1837 
I  followed  Bouillaud  in  Charity  Hospital,  Paris,  and  wit- 
nessed his  coup  S7ir  coup  bleedings  in  this  disease.  It  con- 
sisted in  bleeding  from  the  arm  to  sixteen  ounces  in  the 
morning,  taking  twelve  ounces  by  cup  at  noon,  and  six- 
teen ounces  by  venesection  at  night.  This  practice  was 
repeated  for  two  or  three  days,  so  that  to  abstract  eighty 
to  one  hundred  and  twenty  ounces  of  blood  in  the  course 
of  three  days  was  common  with  him.  He  was  not  indis- 
criminate in  his  application  of  this  treatment,  for  if  the 
patient  was  broken  down,  or  was  of  bad  habits  previous 
to  the  pneumonia,  he  was  not  bled  at  all,  but  was  put  on 
the  tartar  emetic  treatment  so  much  extolled  by  Laen- 
nec.  It  cannot  be  denied  that  many  of  his  patients  lived 
through  it,  possibly  were  cured  by  it.     But  it  was  not 


70  PERICARDITIS. 

just  to  contrast  the  results  of  these  two  modes  of  treat- 
ment, after  the  care  he  exercised  in  the  selection  of  his 
cases.  Physicians  generally  were  not  converted  to  Bouil- 
laud's  plan,  though  at  that  time  they  were  all  bleeders. 
They  seemed  to  think  that  it  was  "  too  much  of  a  good 
thing." 

Eighteen  years,  or  thereabouts,  after  this,  good  old  Dr. 
North,  who  had  retired  from  active  practice,  spent  a*  win- 
ter in  New  York,  and  on  clinical  days  was  always  at  the 
hospital.  By  that  time  the  sanguinary  habits  of  the  pro- 
fession had  been  materially  modified.  Venesection  was 
practised  with  discrimination.  I  had  almost  abandoned 
it  in  hospital  practice,  making,  however,  frequent  use  of 
scarification  and  cups.  The  good  man,  after  hearing  the 
directions  for  the  treatment,  would  fall  back  and,  getting 
the  ear  of  one  of  the  class,  would  say,  ''  This  will  not  do. 
We  cannot  cure  these  men  without  bleeding  from  the 
arm."  At  the  end  of  the  season  I  was  able  to  inform  him 
that  he  had  seen  in  my  wards  forty-three  cases  of  pneu- 
monia, out  of  which  there  were  but  three  deaths.  So 
small  a  mortality  I  then  considered  *'  a  run  of  luck,"  in 
the  character  of  the  cases,  and  have  not  changed  that 
opinion,  for  if  it  was  skill  in  treatment,  that  skill  departed 
from  me  after  that  winter. 

The  late  Dr.  A.  H.  Stevens  had  convinced  himself  that 
the  abstinence  from  venesection  by  the  whole  profession, 
with  the  exception  of  here  and  there  "  an  old-fashioned 
man,"  was  made  necessary  by  a  change  in  the  human  con- 
stitution, and  that  in  his  later  years  man  could  not  bear 
the  bleedings  that  he  witnessed  and  practised  in  earlier 
life.  The  practice  of  the  few  remaining  bleeders;  the 
hemorrhages  of  accidents  and  of  parturition,  with  subse- 
quent recovery,  were  cited  to  him  ;  but  he  would  reply, 
"  You  do  not  know  about  it.  I  have  lived  through  it  all, 
and  know  it  all  well." 


PERICARDITIS.  71 

Subsequent  to  this  conversation  a.  very  striking  case 
occurred,  which,  had  he  witnessed  it,  might  have  shaken 
his  conviction.  A  very  eminent  physician,  when  turned 
of  seventy,  was  attacked  by  pneumonia.  The  lung — it  was 
the  right — was  in  the  crepitant  stage  when  I  first  saw  him 
in  consultation  with  late  Prof.  J.  M.  Smith.  We  had  a 
dozen  leeches  applied  in  the  morning,  and  met  again  in 
the  evening.  -The  first  thing  that  struck  us  on  entering 
the  room  was  the  extraordinary  paleness.  There  was  little 
difference  between  the  color  of  his  face  and  that  of  the  pil- 
low on  which  his  head  rested.  His  expression  was  lan- 
guid. "  It  instantly  occurred  to  us  that  the  leech  bites  had 
been  forgotten  by  the  attendant  and  that  the  patient  was 
bleeding  to  death.  I  at  once  examined  and  found  it  so. 
Our  first  care  was,  of  course,  to  stop  the  bleeding.  I 
pressed  all  the  fingers  I  possessed  on  as  many  leech  bites. 
The  bleeding  was  stopped,  say,  two  minutes.  Then,  turning 
attention  to  the  amount  of  blood  lost,  his  clothes,  includ- 
ing a  flannel  undershirt  on  the  back,  were  saturated.  The 
blood  had  spread  widely  on  the  under  sheet.  From  the 
ticking  of  the  bed  I  removed  three  double  handfuls  of  co- 
agulations. It  had  saturated  two  mattresses  for  a  pretty 
large  space,  and  there  was  a  large  pool  of  blood  on  the 
carpet  under  the  bed.  It  was  impossible  to  ascertain  the 
quantity  he  had  lost  by  any  measurement.  But  that  it 
was  enormous  is  shown  by  what  follows.  We  drew  the 
sheet  out  from  under  him,  and  .after  washing  the  back  in 
warm  water  drew  under  him  an  india-rubber  and  a  linen 
sheet,  having  previously  torn  the  personal  clothing  up 
the  back  and  laid  it  forward.  We  did  not  dare  to  allow 
him  to  sit  up  in  bed.  We  were  about  to  tear  the  fresh 
clothing  up  the  back,  put  his  arms  into  it,  and  tuck  it 
under  the  back.  At  that  point  he  said,  "  Give  the  under- 
shirt to  me.  I  am  strong  enough."  One  of  the  attend- 
ants gave  him  the  shirt  while  our  attention  was  diverted. 


'J2  PERICARDITIS. 

He  partly  raised  himself  in  bed,  and  had  partly  passed 
one  arm  into  a  sleeve  when  he  fell  back  fainting.  When 
he  recovered  his  consciousness  he  willingly  submitted  to 
our  plan.  .  His  pulse  could  scarcely  be  felt,  but  when 
countable  was  140  in  the  minute.  For  days,  indeed  for 
two  or  three  weeks,  even  when  he  could  sit  up,  he  was 
the  palest  man  I  think  I  ever  saw.  This  bleeding  com- 
pletely strangulated  the  pneumonia.  The  crepitation 
ceased  after  a  few  hours,  and  there  was  no  hepatization  at 
all.  There  were  no  remains  of  pneumonia  the  next  day, 
and  no  more  pneumonic  expectoration,  but  he  did  not  re- 
cover from  the  bleeding  for  some  weeks.  This  was,  by 
accident,  heroic  treatment,  and,  so  far  as  the  inflammation 
was  concerned,  was  attended  by  unprecedented  success. 
But  I  have  not  dared  to  follow  its  suggestions. 

Among  the  most  pleasing  books  in  medical  literature 
is  ''  Bartlett  on  the  Certainty  of  Medicine."  In  that 
there  is  a  review  of  the  treatment  of  pneumonia  by 
bleeding,  and  the  author  proves,  as  far  as  anything 
can  be  proved  in  therapeutics,  that  the  practice  diminishes 
the  severity  and  the  mortality  of  the  disease. 

In  the  hospital  I  have  rarely  resorted  to  venesection  for 
two  reasons  :  first,  the  patients  are  most  of  them  per- 
sons whose  health  has  been  impaired  by  the  unwise  use 
of  intoxicating  liquors  or  scanty  or  improper  food.  Sec- 
ond, they  are  likely  to  come  in  at  a  stage  of  the  disease 
in  which  active  treatment  is  harmful.  On  one  occasion  a 
young  woman  of  good  habits  and  of  previous  good  health 
was  admitted,  on  the  third  day  of  pneumonia.  I  asked 
the  house  physician  if  he  had  ever  bled  a  person.  He  had 
not.  Would  you  like  to  bleed  this  patient  ?  He  would 
very  much.  Bare  up  the  arm  and  I  will  guide  you.  But 
he  had  no  lancet.  Other  members  of  the  house  staff  were 
present,  but  none  of  them  had  a  lancet.  There  were  sev- 
eral persons  at  the  clinic — students  and  young  physicians 


PERICARDITIS.  73 

— not  one  of  whom  had  a  lancet.  Not  one  could  be  found 
in  the  hospital  except  among  the  surgical  instruments.  I 
mention  this  occurrence  to  show  what  kind  of  patients 
are  benefited  by  venesection,  and  how  even  then,  fifteen 
or  twenty  years  ago,  bleeding  had  gone  out  of  use  and 
almost  out  of  memory.     ' 

But  in  hospital  practice  I  still  make  constant  use  of 
cups  with  scarifications.  My  private  practice  has  always 
been  limited  to  consultations.  I  have  never  had  a  single 
family.  The  consequence  has  been  that  I  have  rarely  seen 
pneumonia,  or,  for  that  matter,  any  other  disease  till  the 
dangerous  period  had  arrived,  or  for  pneumonia  till  the 
stage  for  active  treatment  had  passed.  Still  my  faith  in 
bleeding  on  the  first  to  the  fourth  day  is  as  active  as  ever. 

When  the  period  for  active  treatment  is  passed,  that  is, 
when  the  consolidation  of  the  lung  has  extended  as  far  as 
it  will,  which,  in  the  majority  of  cases,  Is  at  the  end  of 
the  fifth  day,  it  is  plain  that  the  mischief  is  done.  Bleed- 
ing is  of  no  use  so  far  as  the  consolidated  lung  is  con- 
cerned, but  even  then  it  may  be  called  for  in  aid  of  the 
other  lung,  for  that  other  lung  is  in  danger  of  congestion 
from  the  diversion  of  the  circulation  to  it,  caused  by  ob- 
struction to  the  flow  of  blood  through  the  vessels  of  the 
inflamed  lung,  and  consequent  oedema.  A  moderate 
bleeding  may  help  to  relieve  this  congestion  and  oedema. 
Aside  from  this  we  do  not  entertain  the  question  of 
bleeding,  in  any  way,  after  the  end  of  the  fifth  day,  count- 
ing from  the  initiatory  chill.  But  while  the  disease  is 
passing  from  the  red  hepatization  to  the  gray,  which  every 
pneumonia  must  do  if  the  patient  is  to  get  well,  there  are 
still  active  symptoms.  A  high  temperature  may  require 
sedative  doses  of  quinine,  or  aconite,  or  possibly  veratrum. 
In  many  cases  of  pneumonia  a  condition  of  the  system 
occurs  which  suggests  the  use  of  alcoholic  stimulants.  I 
doubt  whether  they  ever  do  any  good — whether  a  case  that 


74  PERICARDITIS. 

cannot  recover  without  them  will  ever  be  saved  by  giving 
them.  At  the  same  time  I  do  not  think  they  do  harm 
when  properly  used.  What  you  would  do  for  pneumonia 
you  would  do  for  pneumonia  and  pericarditis  combined. 
For  this  pericarditis  there  is  not  a  separate  treatment  un- 
less it  consist  in  giving  moderate  doses  of  an  opiate  to 
quiet  the  irritability  of  the  heart  ;  and  this  may  be  done 
without  fear  of  any  unfavorable  effect  on  the  lungs. 

When  pleurisy  and  pericarditis  concur,  blisters  and  diu- 
retics, which  are  so  effectual  in  pleurisy,  are, not  so  useful, 
as  has  been  said  already,  against  the  pericarditis.  In  ad- 
dition to  these  the  abstraction  of  blood  by  cups  or  leeches 
may  hasten  the  cure  of  the  pericarditis,  especially  as  the 
opiates,  so  useful  in  most  forms  of  that  disease,  may  in- 
terfere with  the  action  of  the  diuretics. 

Pyaemlc  pericarditis  has  a  peculiar  history.  It  appears 
that  a  common  preliminary  is  the  formation  of  small  pus 
spots  in  the  muscles  of  the  heart.  That  those  near  the 
surface  provoke  the  pericarditis,  and  that  the  exudations 
are  there  lymph  and  serum  as  in  the  more  common  form 
of  the  disease.  But  it  sometimes  happens  that  one  or 
more  joi  these  spots  grow  to  a  considerable  size  and  rup- 
ture into  the  pericardial  sac.  The  inflammation  that  fol- 
lows this  accident  is  likely  to  be  attendedby  puralent  exu- 
dation. There  is  little  to  be  said  of  treatment  in  this  va- 
riety of  the  disease.  The  primary  disease  is  so  apt  to  be 
fatal,  and  the  oppression  and  weakness  imposed  on  the 
system  before  the  pericarditis  manifests  itself  is  much 
opposed  to  local  depletion,  and  may  forbid  it.  The  sooth- 
ing Influences  of  opium  suggest  it,  and  it  may  be  used, 
but  not  in  heroic  doses.  When  the  effusion  is  purulent, 
should  the  patient  survive  the  pyaemia,  as  is  quite  pos- 
sible, the  question  of  tapping  will  present  itself. 

Pericarditis  may  occur  independently.  It  is  rare,  but 
a   case   showing   its   possibility  will   soon   be   narrated. 


PERICARDITIS.  75 

When  it  occurs  in  that  manner  the  moderately  free  use 
of  cups  with  scarification,  or  leeches  or  both,  and  of  an 
opiate  will  give  the  best  results.  It  is  common  to  apply 
these  to  the  pericardial  region,  but  as  it  is  not  derivation 
that  is  now  aimed  at,  but  a  moderate  reduction  of  the 
volume  of  the  blood,  it  would  seem  to  be  of  little  impor- 
tance from  what  part  of  the  body  the  blood  is  taken. 
Cups  or  leeches  applied  over  the  heart  do  not  prevent  the 
physical  examinations  which  should  be  duly  made,  as 
blisters  do.  But  blisters  I  am  not  disposed  to  urge.  I 
have  here  a  specimen  which  I  believe  I  have  not  yet 
called  your  attention  to,  and  while  there  is  not  a  word  to 
be  said  regarding  the  treatment  of  such  a  case,  could  it 
be  recognized  during  life  the  curious  fact  which  is  here 
demonstrated  is  worthy  of  your  attention.  You  observe 
first  that  there  is  a  sensible  enlargement  of  the  whole 
heart.  Second,  that  the  pericardium  is  closely  attached 
to  the  organ  everywhere ;  and  third,  that  there  is  a  hoop 
of  calcareous  matter,  firm  as  bone,  completely  investing 
the  heart  in  such  a  way  that  you  would  suppose  the  heart 
could  not  move  either  in  systole  or  diastole.  You  observe 
it  here  over  the  right  auricle  an  inch  in  width  and  an 
eighth  of  an  inch  in  thickness  ;  it  runs  downward  and  to 
the  left  across  the  right  ventricle  on  to  the  left,  about  an 
inch  from  the  apex,  passing  up  the  posterior  of  the  heart 
in  a  line  nearly  parallel  with  that  of  its  descent,  till  it  be- 
comes continuous  with  itself  over  the  right  auricle.  Here, 
as  it  turns  around  the  left  ventricle,  it  has  been  broken  to 
give  admission  to  the  interior  of  the  organ,  and  here  it  is 
formed  into  shape  of  a  rope  and  is  of  the  size  of  the  little 
finger.  You  notice  that  the  structure  is  not  homogeneous 
as  you  would  expect  that  of  bone  to  be,  but  that  the  frac- 
ture is  irregular,  and  parts  are  of  a  whitish  color  and  other 
parts  are  yellowish.  When  it  is  not  broken  you  do  not 
see  it  because  it  is  wholly  within  the  pericardium,  but  you 


yd  PERICARDITIS. 

hear  its  bony  ring  when  I  percuss  it,  and  you  can  feel  it 
and  follow  through  its  whole  circle  as  distinctly  as  you 
can  feel  a  coin  in  your  pocket.  The  pericardium  is  im- 
movably adherent  to  it  throughout,  and  the  heart  by  a 
loose,  thready  tissue. 

The  specimen  came  into  my  possession  without  a  his- 
tor}^,  and  all  we  can  learn  of  the  ante-mortem  facts  must 
be  obtained  from  the  specimen  itself,  and  these  are 
scarcely  enough.  The  evidences  of  a  pericarditis  are 
found  in  this  adhesion  of  the  pericardium  to  the  heart, 
and  that  this  occurred  years  before  death  is  rendered 
probable  by  the  thready  state  of  the  adventitious  mem- 
brane, and  still  more  by  the  presence  of  this  strange 
hoop  that  was  formed  in  all  probability  after  and  in  the 
lymphy  effusion.  It  is  probable  also  that  the  ring  was 
completed  before  it  had  acquired  its  present  breadth  and 
thickness.  In  other  words,  that  it  required  years  to  get 
its  present  dimensions.  Meantime  the  heart  was  beating. 
With  how  much  efficiency  we  can  never  know. 

I  have  never  met  another  that  at  all  resembles  this 
specimen,  and  do  not  remember  that  I  have  seen  a  record 
of  a  similar  case.  But  I  have  not  made  extensive  search 
for  it,  so  that  I  cannot  say  it  is  without  a  parallel  in  mor- 
bid anatomy,  but  it  is  safe  to  say  that  it  is  a  very  rare 
occurrence. 

And  while  we  are  in  the  line  of  rarity  I  will  give  the 
case  alluded  to  a  little  while  ago. 

An  Irish  laborer,  aged  30,  a  well-developed  man,  was 
admitted  into  the  New  York  Hospital  on  i6th  of  Janu- 
ary, 1836.  He  appeared  to  have  had  an  inflammatory 
affection  of  the  chest  tissues  three  weeks  before.  The 
heart  region  was  edematous ;  patient  pale  and  feeble, 
but  not  emaciated;  pulse  130  to  140  in  the  minute  and 
on  exertion  fluttering;  has  cough  attended  by  slight 
expectoration  of  mucus  ;  respiration  oppressed  ;  incapa- 


PERICARDITIS.  7/ 

ble  of  any  exertion — even  turning  in  bed  increases  his 
dyspnoea  and  causes  the  heart  to  flutter;  tongue  but 
sHghtly  furred  ;  bowels  constipated  ;  has  nausea  and  vom- 
its all  ingesta ;  tenderness  of  epigastrium. 

Marked  dulness  in  pericardial  region  and  to  the  right 
and  bft  of  it.  When  the'patient  turns  on  his  right  side 
the  dulness  extends  an  inch  farther  to  the  right  and 
recedes  from  the  left  slightly.  When  he  turns  on  his  left 
side  the  dulness  extends  equally  to  the  left.  Not  the 
slightest  sound  of  respiration  can  be  heard  over  this 
whole  region,  though  distinct  in  other  parts  with  an 
occasional  mucous  rale.  The  impulse  of  the  heart, 
though  not  forcible,  can  be  felt  over  all  this  region  of 
dulness  in  its  calmer  action.  Then  the  sounds  are  nor- 
mal and  its  rhythm  perfect,  most  distinctly  heard  at  the 
base.  The  apex  does  not  strike  against  the  walls  of  the 
chest  in  any  position  of  the  body,  not  even  when  prone. 
A  slight  undulatory  motion  is  perceived  in  the  epigas- 
trium and  in  the  anterior  parts  of  all  the  lower  intercos- 
tal spaces  at  each  pulsation  of  the  heart.  The  action  of 
the  ribs  in  breathing  is  much  restrained. 

There  may  have  been  a  peritonitis,  but  the  man's  pres- 
ent suffering  arises  from  an  enormous  distention  of  the 
pericardium  by  fluid,  and  the  heart's  action  is  crippled  by 
its  pressure  when  exercise  requires  stronger  beats. 

The  nausea  and  vomiting  were  supposed  to  arise  from 
the  condition  of  the  bowels. 

He  improved  on  the  use  of  a  purge,  and  the  nausea, 
and  vomiting  ceased.  Otherwise  the  treatment  was  by 
diuretics. 

This  patient  remained  in  the  hospital  fifty-one  days, 
being  much  of  the  time  able  to  sit  up,  and  sometimes  to 
walk  a  little.  On  the  forty-ninth  day  he  fainted  while  at 
stool,  and  for  two  hours  the  face  and  neck  were  livid ; 
pulse  just  perceptible  at  the  wrist,  but  too  weak  to  be 


7S  PERICARDITIS. 

counted ;  feet  and  hands  cold.  The  next  but  little  im- 
provement ;  pulse  could  be  counted  only  now  and  then, 
for  the  most  part  a  flutter  ;  face  livid  ;  respiration  labored, 
slow,  and  deep  ;  the  mind  clear.  On  the  fifty-first  day 
he  was  found  to  be  dead  one  or  two  minutes  after  his 
pillow  had  been  adjusted.  The  disease  had  lasted,  out  of 
the  hospital  and  in  it,  seventy-two  days.  A  part  of  the 
time  there  had  been  oedema  of  the  feet  and  ankles.  The 
region  of  dulness  was  enlarged  in  the  last  few  days  of  his 
life. 

Autopsy  three  hours  after  death  : 

Face  and  neck  congested  and  livid  ;  surface  over  the 
abdomen,  thorax,  face  and  neck  oedematous  ;  those  of 
legs  and  feet  were  not ;  superficial  veins  bled  freely  when 
cut  ;  some  clear  yellow  serum  in  abdominal  cavity ;  undi- 
gested food  in  the  stomach,  apparently  all  he  had  taken 
in  the  last  two  or  three  days. 

The  liver  was  forced  downward  so  that  its  upper  sur- 
face was  where  its  lower  edge  usually  is,  at  the  free 
border  of  the  ribs.  The  diaphragm  was  forced  downward 
so  as  to  make  a  very  large  convexity  downward  into  the 
abdomen. 

The  distended  pericardium  was  loose  and  hard,  occupy- 
ing the  whole  anterior  of  the  chest  and  extending  out  of 
view  on  each  side  when  the  sternum  and  cartilages  were 
removed.  It  extended  backward  to  the  spinal  column 
and  downward  so  as  to  form  the  pouch  in  the  diaphragm 
»and  depress  the  liver  as  stated  above.  Each  lung  was 
pressed  into  the  posterior  and  upper  portion  of  the 
thorax.  The  edges  of  the  lungs  were  adherent  to  the 
pericardium  on  each  side.  A  small  quantity  of  fluid  was 
found  in  each  pleuritic  cavity.  The  lungs  were  healthy 
but  compressed. 

The  pericardium  when  opened  was  found  to  be  one 
eighth  of  an  inch  in  thickness  and  to  have  a  firm,  leathery 


PERICARDITIS.  79 

feel,  and  contained  a  gallon  of  clear  yellbw  serum.  There 
was  a  thick  covering  of  lymph  over  all  the  heart  and  all  the 
inner  surface  of  the  pericardium.  The  two  were  united 
by  tendinous  threads  and  bound  posteriorly  and  anteri- 
orly. There  had  been  adhesion  of  the  pericardium  to  the 
heart  anteriorly,  as  was  evident  from  patches  of  lymph 
found  on  one  surface,  removed  from  one  surface  and 
found  on  the  other,  and  from  flakes  of  lymph  attached 
by  one  edge  of  the  floating  fin  and  by  broken  threads  so 
attached.  The  deposits  on  the  anterior  of  the  heart  were 
stained  with  blood  effused  underneath  them. 

This  case  is  copied  from  the  New  York  Hospital  Rec- 
ord Book,  and  was  then  written  by  myself  soon  after  the 
date  given  above.  There  are  two  other  facts  relating  to 
the  case  which  are  not  there  recorded,  both  of  which  are 
as  distinct  in  my  mind  as  if  the  case  had  occurred  yester- 
day. How  the  first  escaped  record  I  cannot  explain,  ex- 
cept on  the  supposition  of  haste,  as  house  physicians  then 
as  now  were  crowded  with  ward  and  other  work  and  had 
little  time  for  "  writing  up  cases."  The  second  was  pur- 
posely omitted,  because  it  might  have  been  regarded  as 
an  improper  criticism  by  an  inferior  on  the  judgment  of 
his  superior. 

The  first  of  these  facts  was  that  in  the  last  week  of  the 
patient's  life,  after  the  dulness  was  found  to  be  extend- 
ing, the  sternum  was  found  broken  up  into  several  pieces, 
which  were  movable  by  pressure  of  the  finger,  one  on 
another.  I  cannot  say  that  it  was  a  disunion  of  its 
natural  subjoints.  It  seems  to  me  that  the  fragments 
were  of  irregular  shape,  but  of  the  breaking  up  of  the 
sternum  I  have  no  doubt.  The  second  fact  is  that  I 
asked  the  two  attending  physicians  in  succession  for  per- 
mission to  tap  the  pericardium.  They  both  declined  to 
perform  the  operation,  or  to  permit  me  to  perform  it, 
and  when  at  length  the   patient  had  nearly  reached  the 


So  PERICARDITIS. 

"  in  extremis"  I  applied  to  the  superintendent  for  his 
sanction  of  the  operation,  but  he  declined  to  give  it 
because  he  was  not  a  physician  and  had  no  control  in  the 
medical  administration  of  the  hospital,  and  so  the  patient 
died,  and  probably  would  have  died  if  the  operation  had 
been  performed  at  that  late  period  of  his  disease.  This 
would  not  have  been  strictly  a  new  operation,  as  will  be 
seen  hereafter,  but  was  then  wholly  unknown  to  the 
hospital  physicians  and  probably  to  the  whole  profession' 
in  this  country. 

Tappmg  the  Pericardium. — In  vastly  the  greater  num- 
ber of  cases  in  which  inflammatory  action  has  caused  fluid 
effusion  into  the  pericardial  sac,  the  question  of  tapping 
does  not  arise.  Every  physician  has  been  surprised  in 
observing  how  quickly,  after  the  inflammation  has  begun 
to  subside,  the  fluid  disappears.  Such  cases  take  care  of 
themselves,  and  there  is  but  little  respiratory  oppression, 
and  what  there  is  is  of  short  duration.  In  such  cases 
the  question  of  tapping  is  not  entertained.  When  the 
fluid,  however,  compresses  the  heart  and  obstructs  the 
entrance  of  blood  by  the  venae  cavae,  and  encroaches  on 
the  breathing  space  by  its  bulk,  when  the  patient's  life  is 
in  danger  by  the  quantity  of  the  fluid,  then  I  must  urge  as 
I  did  in  the  case  just  narrated,  that  tapping  is  positively 
demanded.  But  is  there  not  danger  of  wounding  the 
heart  ?  Undoubtedly,  and  it  was  for  this  reason  the  earlier 
operators  opened  the  pericardium  with  bistoury  and 
scissors,  instead  of  a  trocar.  But  regarding  these  wounds, 
the  experience  of  New  York  surgeons  in  the  last  thirty 
years  has  in  some  degree  diminished  the  dread  of  them. 
One  man  was  shot  through  the  heart  and  lived  several 
days.  After  death  the  bullet  was  found  in  one  of  its 
cavities.  Another  man  lived  eighteen  or  twenty  days 
after  a  bullet  had  been  lodged  in  the  septum  ventricu- 
lorum.     Of  late   the   right    auricle   has   been    purposely 


PERICARDITIS.  8 1 

penetrated  by  a  hollow  needle  for  the  depletion  of  this 
cavity,  and  it  is  said  that  the  patient  was  temporarily 
improved  by  the  operation.  Still  we  all  feel  that  no 
fool's  play  can  be  permitted  about  the  heart,  and  it  is  the 
aim  of  every  operator  to  enter  the  pericardium,  and  at  the 
same  time  avoid  the  heart.  In  almost  all  the  cases  requir- 
ing tapping,  when  the  patient  is  in  the  prone  position, 
the  heart  falls  backward  to  the  posterior  limit  of  the  sac, 
and  the  fluid  comes  in  anteriorly  between  the  sac  and  the 
heart.  The  depth  of  the  fluid  in  this  position  varies  from 
half  an  inch  to  an  inch  or  more.  It  is  possible  to  pene- 
trate the  pericardium  anteriorly,  and  yet  stop  short  of 
the  heart  itself.  Otherwise,  choose  a  point  which  the  dis- 
tended pericardium  occupies,  but  which  is  off  the  Hmits 
of  the  heart. 

Dr.  John  B.  Roberts,  in  1880,  published  a  volume 
entitled  Paracentesis  of  the  Pericardium,  in  which  he 
gives  a  table  of  all  the  cases  in  which  this  operation  had 
been  performed  at  that  time,  so  far  as  he  could  rely  on 
the  printed  reports.  He  finds  in  all  sixty,  in  these  the 
point  of  insertion  was  the  third  intercostal  space  in  2  ; 
the  fourth  in  22 ;  the  fifth  in  18  ;  the  sixth  in  5,  making 
47  in  which  the  point  of  insertion  is  stated.  Those  made 
in  the  third  and  fourth  spaces  were  over  the  heart ;  those 
in  the  fifth  would  have  a  good  chance  of  escaping  the 
heart,  especially  if  made  against  the  upper  border  of  the 
sixth  rib ;  and  those  in  the  sixth  would  be  nearly  certain 
of  being  off  it,  unless  the  organ  was  enlarged.  In  these 
sixty  cases  there  were  twenty-four  recoveries.  These  are 
distributed  as  follows  :  Of  the  two  in  the  third  space,  o ; 
of  the  twenty-two  in  the  fourth,  10 ;  of  the  eighteen  in  the 
fifth,  9 ;  of  the  five  in  the  sixth,  2.  So  three  of  the  recov- 
eries belong  to  the  cases  in  which  opening  was  performed 
by  bistoury  and  scissors,  or  those  in  which  the  place 
of  tapping  is  not  stated.     Success  is  about  equally  divided 


82  PERICARDITIS. 

between  the  fourth  and  fifth  spaces.  With  the  fifth  the 
recoveries  were  just  one  half,  for  the  fourth  a  fraction 
less,  or  -f^.  Twenty-four  recoveries  in  sixty  operations 
does  not  seem  to  be  a  brilliant  success,  but  if  we  can 
suppose  that  twenty-four  persons  by  this  means  were 
really  snatched  from  death,  it  assumes  another  aspect.  I 
have  not  attempted  to  look  up  and  read  up  the  cases 
which  Dr.  Roberts  has  tabulated,  but  if  many  of  them 
were  rescued  from  a  condition  anything  like  that  which 
is  detailed  of  the  case  in  the  New  York  Hospital,  where 
I  implored  permission  to  tap  the  patient,  the  operation 
has  accomplished  little  less  than  resurrection. 

Dr.  William  Pepper's  case  {Am.  Jour,  of  Med.  Science^ 
April,  1879,)  resembled  mine  in  severity,  with  this  differ- 
ence, that  mine  was  inoribund  and  left  to  die,  his  "  was 
evidently  moribund,"  was  tapped  and  recovered,  so  far 
as  the  cardiac  effusion  was  concerned,  and  died  fifteen 
months  later  of  an  unusual  form  of  disease  of  the  serous 
membranes.  The  same  diathesis  which  produced  the  lat- 
ter may  have  and  probably  did  produce  the  pericarditis, 
but  at  the  inspection  the  pericardial  cavity  was  wholly 
obliterated  by  adhesions,  and  appeared  to  have  nothing 
to  do  with  the  fatal  issue.  He  began  with  a  most  dis- 
couraging case,  but  he  brought  it  out  triumphantly. 

His  trocar  was  inserted  "in  the  fifth  intercostal  space 
about  one  inch  inside  of  the  line  of  the  left  nipple,  i.e., 
nearly  in  the  normal  position  of  the  apex  beat,  and  over 
eight  ounces  of  reddish  serum  were  removed."  Relief 
was  immediate,  recovery  was  slow  and  incomplete,  as  she 
was  weighed  down  by  other  disease. 

As  to  the  mode  of  operation,  whether  by  what  is  now 
called  "  aspiration"  or  by  the  old-fashioned  trocar  is  not 
very  emphatically  taught  by  Dr.  Roberts'  table.  Of  his 
whole,  sixty,  thirty-six  died.  Among  these  sixty, 
"  aspiration"    was   practised    in   twenty-four.     Of   these, 


PERICARDITIS.  83 

ten  recovered  and  fourteen  died ;  or,  in  figures,  f  of  the 
whole  died,  and  y'^  of  those  who  were  "aspirated." 
*' Aspiration"  of  the  pericardium  does  not  appear  to  have 
been  practised  till  about  fifteen  years  ago.  Since  then  it 
has  been  preferred  by  most  operators  to  the  trocar,  and 
it  may  be  that  a  better  knowledge  of  the  operation  gives 
it  its  apparent  advantage.  Dr.  Roberts  professes  a  de- 
cided preference  for  it.  'He  would  have  the  receiver  ex- 
hausted of  air  beforehand,  the  penetrating  instrument 
introduced  slowly,  and  the  whole  so  arranged  that  the 
operator  can  see  the  first  drops  of  fluid  that  escape  from 
the  sac,  and  thus  avoid  penetrating  too  deeply.  Dr. 
Roberts  considers  the  "  Point  of  Puncture"  at  some 
length,  and  holds  that  one  of  two  should  be  preferred — 
"  the  fossa  between  the  ensiform  and  the  costal  carti- 
lages of  the  left  side,  and  the  fifth  intercostal  space  near 
the  junction  of  the  sixth  rib  with  its  cartilage,"  and  after 
some  reasoning  he  adds:  "Therefore  I  should  tap  in  the 
former  position  as  a  rule,"  i.e.,  the  fifth  left  space,  "  re- 
serving the  latter"  left  xiphoid  fossa  "  for  special  cases, 
where  there  was  some  indication  for  making  an  ex- 
ception." 

In  such  a  case  as  that  in  the  New  York  Hospital  the 
puncture  might  be  made  almost  anywhere  in  the  front  of 
the  chest  below  the  fourth  rib,  for  the  sac  extended  as 
much  to  the  right  as  to  the  left,  while  the  heart  kept  its 
proper  position.  In  such  a  case,  "  Dr.  Robert's  suggestion 
to  tap  on  the  right  side  of  the  sternum  in  the  fifth  space, 
about  four  and  a  half  to  five  centimetres  from  the  edge 
of  the  sternum,"  would  be  safe  and  proper.  But  suck 
cases  are  extremely  rare,  if  indeed  another  gallon  sac  has 
been  seen  by  anybody.  But  any  pericardial  effusion  that 
produces  distress  enough  to  raise  the  question  of  tapping 
will  be  very  exceptional  if  it  does  not  extend  to  the  right 
as  well  as  to  the  left,  and  how  far  it  is  easy  to  ascertain. 


84  PERICARDITIS. 

You  are  too  fresh  from  your  anatomy  to  make  it  needful 
that  I  point  out  the  danger  of  wounding  the  internal 
mammary  artery. 

Tapping  the  Pericardium — Recovery. — It  was  in  the 
Leeds  Infirmary,  service  of  Dr.  AUbut,  case  reported  by 
the  house  physician,  and  published  in  the  Lancet,  Janu- 
ary 27,  1882.  The  patient,  twenty-two  years  of  age.  He 
had  had  rheumatic  fever  six  or  seven  years  before.  He 
was  admitted  December  23,  1883,  with  pains  in  his  joints, 
not  undoubtedly  rheumatic.  Salicylate  of  soda  did  not 
relieve  him ;  seemed  to  produce  some  delirium  (20  grs. 
every  two  hours)  and  was  discontinued.  Had  pleurisy 
on  the  23d  of  January;  he  had  been  steadily  improving 
for  the  last  four  or  five  days.  This  morning  he  is  pale 
and  breathing  rapid ;  not  in  any  great  pain,  but  a  little 
discomfort  in  the  breathing;  cardiac  dulness  much  in- 
creased. It  begins  at  the  third  rib  and  extends  down- 
ward to  the  sixth,  and  is  much  increased  to  the  right  of 
the  sternum,  distinct  friction  fremitus  felt  over  the  up- 
per part  of  dulness,  friction  sound  heard  over  upper  half 
of  dulness,  the  systolic  portion  of  which  was  double ;  pulse 
130,  evening  temp.  100.6°. 

Feb.  2. — Pericardial  effusion  rather  increased.  The 
praecordial  region  has  a  full  distended  look,  no  intercostal 
sinking.  The  absolute  dulness  begins  now  almost  at  the 
second  rib,  and  extends  down  to  the  seventh,  laterally  on 
the  fourth  rib  it  measures  eight  inches ;  heart  sounds 
obscure  and  distant ;  no  friction  sound  now.  To-day  for 
the  first  time  the  epigastrium  is  full  and  tender,  and  dull 
on  gentle  percussion.  The  edge  of  the  liver  on  the  level 
of  the  umbilicus.     Temperature,  100°;  pulse,  128. 

Feb.  7. — It  is  evident  that  he  cannot  hold  out  much 
longer  if  present  condition  continues.  A  fine  aspirator 
needle  was  introduced  in  the  fourth  left  space,  two  inches 
and  a  half  from  the  median   line,  directed  upward  and 


PERICARDITIS.  8$ 

backward  until  a  cavity  was  clearly  entered  at  the  depth 
of  an  inch  and  a  half.  Only  about  an  ounce  of  bloody 
turbid  serum  could  be  drawn  off.  It  was  not  till  the  nth 
that  the  patient  began  to  mend.  He  continued  to  im- 
prove, and  left  the  hospital  May  i8. 

It  may  be  that  the  withdrawing  of  an  ounce  of  fluid  in 
this  case  relieved  pressure,  and  so  favored  absorption. 
Every  physician  of  large  practice  has  seen  this  kind  of 
relief  in  pleurisy.  A  patient  has  one  pleural  cavity  filled, 
distended  with  serum.  He  tries  blisters  and  diuretics  in 
vain.  I  have  tried  all  approved  means  for  two  months 
without  making  any  favorable  impression.  A  portion 
of  the  fluid  is  then  drawn  off,  and  it  need  not  be 
a  large  portion;  directly  the  same  agents  that  were  in 
operation  before  become  effective,  and  the  fluid  is  ab- 
sorbed in  a  few  days.  That  Dr.  Albutt's  patient  was 
relieved  by  absorption  needs  no  argument.  Whether 
the  absorption  would  have  occurred  without  the  tapping 
may  be  a  question.  The  statement  I  have  quoted,  "  It 
is  evident  he  cannot  hold  out  much  longer  if  the  present 
condition  continues,"  has  an  important  bearing  on  this 
point.  If  there  are  cases  in  which  the  removal  of  a  part 
of  the  fluid  will  determine  the  absorption  of  the  remainder, 
such  cases  will  be  a  sort  of  counterpoise  to  those  that- re- 
quire repeated  tappings. 

Signs  of  Pericardial  Adhesions. — On  this  topic  there  has 
been  a  great  deal  of  fine  reasoning,  and  some  good  obser- 
vation, but  observation  and  apparently  good  observation 
varies  widely  in  results.  Indeed  the  cases  must  vary  one 
with  another.  I  have  already  shown  specimens  in  which 
the  pericardium  is  closely  and  firmly  adherent  to  the 
heart,  so  that  the  pericardium  must  make  every  movement 
that  the  heart  makes,  and  have  shown  how  this  kind  of 
adhesion  produces  a  twisting  movement  in  the  diaphragm. 
I  have  also  shown  you  specimens  in  which  the  adhesion 


S6  PERICARDITIS. 

was  not  an  adhesion,  though  it  was  at  one  time.  The 
plastic  matter  had  been  drawn  out  into  threads  half  an 
inch  long,  by  the  interposition  of  serum.  The  serum  re- 
maining more  than  the  usual  time  the  plastic  matter  may 
lose  its  adhesiveness,  and  the  cormection  be  kept  up  by 
threads  only.  Again  you  have  seen  when  close  adhesions 
are  breaking  down,  the  last  stage  is  marked  by  a  multi- 
tude of  very  fine  threads  running  from  the  pericardium 
to  the  heart,  and  both  cleared  of  false  membrane  except 
at  the  points  of  attachment  of  these  threads.  In  either 
of  these  cases  the  heart  has  its  natural  play  without  drag- 
ing  the  pericardium  after  it.  In  the  case  of  dissolving  ad- 
hesions you  will  rarely  understand  that  a  set  of  symptoms 
indicating  adhesion  may  have  lasted  one  or  more  years  and 
then  have  gradually  disappeared. 

Still  again  you  have  seen  instances  of  close  adhesion, 
perhaps  equally  close,  while  the  hearts  varied  greatly  in 
the  quantity  and  quality  of  their  muscular  fibres.  Here, 
for  example,  is  a  cor  bovinis,  hypersarcosis  cordis ;  and  here 
is  one  that  is  not  hypertrophied,  but  of  natural  size  ;  the 
pericardium  is  closely  adherent  to  each.  The  power  of 
one  is  double,  perhaps  triple,  that  of  the  other.  This  is 
not,  perhaps,  felt  in  the  vessels  because  there  is  a  grave 
obstruction  at  the  aortic  valve  but  it  is  exerted  in  the 
chest  and  felt  in  its  walls  and  will  give  signs  of  its  pres- 
ence that  the  heart  of  normal  size  cannot  give.  Here  is 
still  another  ;  it  is,  perhaps,  under  size,  but  I  will  not  make 
a  point  of  that ;  it  is  clearly  not  enlarged,  but  it  is  yellow- 
in  color,  in  consistency  flabby  and  soft.  It  is  an  instance 
of  the  oily  degeneration  of  the  muscular  fibres  of  the 
heart.  The  pericardium,  you  see,  is  closely  attached  as  in 
the  others.  But  you  would  expect  during  Hfe  no  signs  of 
this  adhesion  whatever. 

There  is  another  point  in  this  history  which  is  of  great 
importance.     It  is  said  that  when  the  serous  pericardium 


PERICARDITIS.  8/ 

is  inflamed  the  diseased  action  shows  a  disposition  to 
penetrate  the  whole  thickness  of  the  sac,  and  appear  on 
its  outside,  and  that  the  result  of  this  action  is  often  a 
firm  adhesion  of  the  pericardium  to  the  inner  surface  of 
the  sternum  and  of  the  costal  cartilages.  That  this  does 
occur  cannot  be  denied,  but  as  to  its  frequency  I  may 
state  that  most  of  numerous  specimens  by  means  of  which 
I  have  demonstrated  to  you  the  various  phases  of  peri- 
carditis were  removed  from  the  body  by  my  own  hand  or 
under  my  immediate  direction,  and  that  when  the  ster- 
num has  been  separated  from  the  clavicles  and  the  carti- 
lages from  the  bony  ribs  the  raising  of  these  was  an  easy 
work;  a  few  broad,  careless  sweeps  of  the  knife  have  sun- 
dered the  scanty  connections  of  the  sternum  and  its  ap- 
pendages to  the  parts  within.  It  has  rarely  been  neces- 
sary to  make  careful  dissection  to  separate  the  pericar- 
dium from  these  parts.  But  when  such  adhesions  exist, 
they  certainly  have  very  telling  effects  among  the  signs  of 
pericardial  adhesion. 

It  comes  then  to  this :  the  most  marked  of  these  signs 
will  be  observed  when  the  adhesions  are  close,  when  the 
heart  is  hypertrophied  and  strong,  and  when  strong  at- 
tachment exists  between  the  anterior  of  the  pericardium 
and  the  inner  face  of  the  sternum  and  cartilages,  and  that 
there  will  be  feeble  external  signs  when  such  expericardial 
attachments  do  not  exist  and  the  heart  is  of  usual 
strength,  and  none  at  all  when  the  heart  is  feeble,  whether 
the  expericardial  attachments  exist  or  not. 

In  consideration  of  these  points  the  following  can  be 
understood : 

In  a  case  in  which  it  was  all  but  certain  that  these  ad- 
hesions existed,  and  in  which  they  were  found  to  be 
"  close  and  universal,"  after  death.  Dr.  Wm.  Pepper 
sought  for  such  evidences  as  have  been  supposed  to  prove 
it.     *'  But  in  fact  they  were  entirely  absent.  The  impulse 


88  PERICARDITIS. 

of  the  heart  was  diffused  and  feeble,  and  unattended 
with  thrill.  There  was  no  recession  of  the  intercostal  tissue 
during  the  ventricular  systole,  nor  any  diastolic  collapse 
of  the  jugular  veins,  nor  recession  of  the  epigastrium.  And 
this  was  the  case  despite  the  fact  that  there  existed  those 
external  adhesions  between  the  pericardium  and  the  chest 
wall  in  front,  which  seem  in  some  cases  to  render  the  above 
mentioned  signs  of  pericardial  adhesion  more  evident. 
This  case  must  be  regarded  as  another  illustration  of  the 
fact  that  while,  when  these  signs  are  present,  the  existence 
of  adherent  pericardium  may  be  assumed  with  great  prob- 
ability. They  may  all  be  absent  in  cases  of  complete  ad- 
hesion.** 

Another  observer,  writing  in  the  Union  Medicate,  re- 
lates a  case  apparently  of  tapping  the  pericardium  and 
states  that  ''  the  doubtful  position  and  value  of  this  op- 
eration makes  the  case  of  interest.  The  patient  suffered 
from  a  pericarditis  with  effusion,  produced  by  exposure 
to  cold.  The  symptoms  of  pressure  were  severe  ;  a  punc- 
ture was  made  and  a  little  fluid  removed.  A  month  later 
the  patient  had  double  pleurisy.  He  finally  recovered 
with  pericardial  adhesions."  (The  Med.  Record,  Jan.  6, 
1883.) 

Dr.  Sibson,  in  ''  Reynolds'  System  of  Med.,"  who  has 
written  elaborately  if  not  lucidly  on  these  signs,  says : 
"The  discovery  of  adherent  pericardium  during  life  is  in 
some  cases  impossible  ;  in  some  doubtful  or  difficult ;  but 
in  otherS;  and  these  are  among  the  most  important  cases, 
its  existence  can  be  ascertained  during  life,  on  reasonable 
and  well-ascertained  grounds. 

"  When  the  adhesions  are  partial,  or  when  the  heart, 
though  completely  adherent,  is  small,  is  not  bound  by 
external  adhesions  to  the  anterior  walls  of  the  chest,  and 
is  covered  to  the  natural  extent  by  the  lungs,  their  ex- 
pansion being  free  and  unconstrained,  then  the  varying 


PERICARDITIS.  89 

relation  of  the  heart  and  lungs  to  the  chest  is  quite 
natural,  and  the  diagnosis  of  the  adhesions  is  impossible. 
If  the  adherent  heart  be  enlarged,  and  is  not  attached  to 
the  lower  half  of  the  sternum  and  the  cardiac  cartilages 
by  combined  pericardial  and  pleural  adhesions,  so  that 
the  active  or  automatic  and  passive  or  respiratory  move- 
ments of  the  heart  are  scarcely  or  but  little  interfered 
with,  the  inspiratory  expansion  of  the  lungs  is  freely  per- 
mitted, and  the  diagnosis  of  the  adherent  pericardium 
may  be  difficult,  obscure,  or  even  impossible. 

*'  When,  however,  the  heart  is,  as  usual,  enlarged,  being 
often  affected  with  valvular  disease,  the  adhesions  may 
be  short,  fibrous,  and  binding ;  and  the  front  of  the  organ 
may  be  fixed  to  the  two  lower  thirds  of  the  sternum  and 
the  adjoining  cartilages  by  pleuro-pericardial  adhesions, 
so  that  the  automatic  and  respiratory  movements  of  the 
heart  and  the  inspiratory  expansion  of  the  lungs  are  re- 
strained:  thus  the  discovery  of  the  adhesions,  during  life, 
may  generally,  in  such  cases,  be  made  by  a  careful  study 
of  the  physical  signs ;  its  diagnosis  being  the  more  cer- 
tain and  easy  in  proportion  as  the  heart  is  more  enlarged 
and  more  firmly  fixed  to  the  anterior  walls  of  the 
chest." 

Puncture  and  Suture  of  the  Heart. — Dr.  Roberts  read  a 
paper  at  a  meeting  of  the  Philadelphia  College  of  Physi- 
cians, in  which  he  cites  some  instances  in  which  the  heart 
has  been  punctured  when  the  purpose  was  to  tap  the 
pericardium,  and  claims  that  these  accidental  punctures 
did  no  harm,  and  calls  attention  to  Dr.  Westbrook's 
paper  (published  in  the  Medical  Record,  Dec.  23,  1882),  in 
which  he  describes  an  intentional  tapping  of  the  right 
auricle  to  relieve  a  heavy  congestion,  and  urges,  that  if  a 
few  drachms  of  blood  taken  from  the  heart  will  give  as 
much  relief  as  the  same  number  of  ounces  taken  from,  the 
arm,  it  is  a  great  economy  of  blood. 


90  ^  PERICARDITIS. 

He  thinks  also  that  important  results  will  follow  Dr. 
Block's  experiments  on  animals,  which  show  that  in  them 
not  only  can  the  pericardium  be  opened  to  remove  clots  of 
blood,  but  that  opening  the  right  or  left  ventricle  and 
entire  compression  of  the  heart  for  the  application  of 
suture  can  be  supported  by  rabbits  for  several  minutes. 
Even  if  the  cardiac  pulsation  and  breathing  stop  during 
the  operation,  death,  he  asserts,  does  not  necessarily  fol- 
low, (For  Dr.  Block's  experiments  see  Jour,  of  Med. 
Science,  Jan.,  1883,  p.  274;  N.  Y.  Medical  Journal,  March 
17,  1883.) 

Pericardial  Puncture  and  Incision  and  Drainage. — At  a 
meeting  of  the  Royal  Medical  and  Chirurgical  Society, 
Dr.  Samuel  West  reported  the  case  of  a  boy,  16  years  of 
age,  who  had  a  large  pericardial  effusion.  The  symptoms 
became  so  urgent  that  paracentesis  was  performed.  Pus 
was  obtained.  Three  days  later  paracentesis  was  again 
performed,  and  subsequently  the  pericardium  was  laid 
freely  open,  evacuated,  washed  out,  and  a  drainage-tube 
inserted.  The  boy  recovered  completely  in  five  weeks, 
having  had  in  the  meantime  an  attack  of  urticaria.  The 
place  selected  for  the  operation — puncture — was  the 
fourth  intercostal  space,  immediately  behind  the  left 
nipple.  The  amount  of  fluid  obtained  at  the  first  tap- 
ping was  fourteen  ounces ;  by  the  incision,  two  quarts. 
There  was  a  peculiar  epigastric  prominence  noticed  before 
the  paracentesis,  which  disappeared  after  the  operation. 
The  pulsus  paradoxis  was  constant  till  the  free  incision 
was  made,  and  ceased  immediately  after  that. 

Dr.  West  then  gave  a  short  account  of  the  only  other 
recorded  case  of  incision  of  the  pericardium  for  purulent 
pericarditis,  by  Prof.  Rosenstein,  of  Leyden,  which  also 
recovered. 

Dr.  West  then  gave  a  history  of  the  operation.  It 
was  first  suggested  in    1649.    It  was   first  practised   in 


PERICARDITIS.  9I 

Barcelona,  in  two  cases.  In  1841  there  was  a  remark- 
able series  of  cases  in  an  outbreak  of  scurvy  in  Russia, 
in  which  the  pericardial  effusion  was  mostly  blood. 
Nine  were  operated  on,  and  six  recovered.  In  1854 
Trousseau's  essay  was  published  upon  some  cases  of 
his  own  and  of  Mr.  Aran,  which  revived  an  interest  in 
the  subject.  In  1866  Dr.  Clifford  Allbutt  introduced  the 
operation  into  England,  and  it  was  performed  by  Wheel- 
house  and  Mr.  Teale.  Rosenstein,  in  1871,  made  the  ad- 
vance, in  opening  the  pericardium  by  incision  with  drain- 
age. A  list  of  recorded  cases,  including  some  hitherto 
unpublished,  was  given  in  a  tabular  form,  making  79 
cases  in  all.  .  .  . 

Phthisis  and  pleurisy  were  associated  with  23 ;  rheu- 
matism with  II  ;  scurvy  with  9;  general  dropsy  with  5  ; 
injury  with  3;  in  12  there  was  no  associated  disease. 
The  amount  of  fluid  evacuated  was  in  46  cases  less  and 
in  38  more  than  a  pint.  The  larger  quantity  was  in  the 
scorbutic  cases,  and  from  one  of  these  about  ten  pints 
was  obtained.  Dieulafoy  selected  the  fifth  left  space, 
about  an  inch  from  the  sternum,  as  the  safest  point  for 
puncture.  Only  one  case  is  recorded  in  which  the  opera- 
tion was  fatal.     {A7fi.  Jour,  of  Med.  Sci.,  July,  1883.) 

Penetrating  the  Right  Ventricle. — On  the  presentation 
of  Dr.  West's  case  of  pericardial  puncture  and  incision, 
Dr.  Hulke  said  that  he  considered  it  advisable  to  dissect 
down  carefully  to  the  pericardium  before  any  incision 
was  made,  and  if  a  trocar  and  canula  were  employed,  he 
advised  a  very  careful  use  of  them,  and  that  the  trocar 
be  frequently  withdrawn  to  form  an  opinion  of  the  parts 
reached.  He  had  himself,  after  medical  consultation,  in 
a  case  that  was  believed  to  be  one  of  pericardial  effusion, 
once  inserted  a  trocar  and  canula  somewhat  boldly,  and 
the  withdrawal  of  the  trocar  had  been  followed  by  a  jet 
of  blood  which  gave  him  great  alarm,  but  happily  relieved 


92  PERICARDITIS. 

the  patient.  A  subsequent  post-mortem  examination 
showed  him  that  he  had  punctured  the  right  ventricle, 
and  that  the  case  was  one  of  universally  adherent  peri- 
cardium.    {Am.  Jour,  of  Med.  Sci.,  July,  1883,  p.  264.) 

Dr.  Partzersky  is  reported  {Am.  Jour.  Med.  Set.,  April, 
1883)  to  have  brought  before  the  Moscow  Physico- 
Medical  Society  a  very  interesting  case  of  pericardial 
effusion,  treated  by  repeatedly  performed  tapping,  and 
finally  by  incision  of  the  pericardial  sac,  with  subse- 
quent drainage.  These  are  the  author's  views:  I.  In 
a  vast  majority  the  operation — that  is,  puncture  and 
aspiration,  and,  if  they  fail,  subsequent  incision  with 
drainage — is  not  attended  with  any  danger.  2.  It 
brings  rapid  relief,  and  its  palliative  usefulness  is  ad- 
mitted. 3.  In  the  absence  of  such  complications  as 
tubercles,  cancer,  organic  changes  of  the  heart,  etc.,  the 
operative  treatment  of  non-purulent  pericardial  effusions 
may  prove  successful  in  the  majority  of  cases.  4.  In 
purulent  pericarditis  an  early  operation  is  justifiable,  in 
order  to  prevent  dilatation  and  fatty  degeneration  of  the 
heart,  which  generally  supervenes  very  rapidly. 

Cancer  of  the  (Esophagus  Producing  Pericarditis  and 
Pneumo-Pericardium. — There  had  been  a  steadily  increas- 
ing difficulty  in  swallowing,  in  a  woman  of  43,  for  many 
months.  There  was  much  regurgitation  of  food.  At 
length  the  to-and-fro  sound  of  pericarditis  was  recog- 
nized. Six  days,  after  a  churning  splashy  a  resonant  per- 
cussion indicated  that  air  had  entered  the  pericardium. 
She  died  two  days  later,  and  it  was  found  that  a  cancer 
— (epithelioma  ?) — had  made  extensive  ravages,  and  had 
penetrated  the  posterior  of  the  pericardium  so  as  to 
make  an  opening  that  admitted  the  point  of  the  finger. 

Dr.  Begbie  reviews  the  history  of  pneumo-pericardium, 
and  recognizes  three  different  ways  in  which  it  may  be 
produced:   I.  It  may  be  secreted.     2.   It  may  result  from 


'  PERICARDITIS.  '  93 

decomposition  of  fluid  in  the  pericardium(?).  3.  It  may 
by  perforation  be  admitted,  whether  that  is  caused  by 
disease  or  injury. 

That  a  gaseous  matter  may  be  secreted  under  such 
conditions  I  believe  is  possible,  both  from  the  reliableness 
of  those  who  have  recorded  such  cases  and  from  one  that 
I  have  myself  seen.  Dr.  Stokes  has  seen  one  such  case, 
and  Laennec  thought  it  Was  a  common  occurrence  in  the 
dying,  and  he  has  given  accurately  the  physical  indication 
of  it.  If  this  mode  of  production  is  admitted,  then  the 
gaseous  decomposition  of  the  contents  of  the  pericardium 
is  rendered  doubtful.  Bricheleau  did  indeed  meet  with 
one  case  of  pneumatosis  of  the  pericardium,  and  on  post- 
mortem examination  the  pus  found  in  the  cavity  was 
found  to  be  very  fetid.  But  even  in  such  a  case  it  is  as 
easy  to  suppose  that  the  gas  was  carbonic  acid  gas  elim- 
inated from  the  blood-vessels  as  it  is  in  the  intestinal 
tube,  and  taking  the  odor  of  the  fetid  contents  of  the  sac 
in  the  same  way  that  an  abscess  in  contact  with  an  intes- 
tine acquires  a  faecal  odor  without  faecal  admixture,  as  it 
is  to  admit  gaseous  decomposition.  Into  the  third  class 
falls  a  case  mentioned  by  Dr.  Graves,  in  which  a  communi- 
cation between  the  stomach  and  pericardium  was  pro- 
duced by  an  abscess  of  the  liver  which  opened  into  both, 
and  one  by  Dr.  Flint,  in  which  the  patient  was  stabbed 
with  a  knife,  which  made  a  slight  opening  in  the  peri- 
cardium ;  one  by  Dr.  Walshe,  in  which  a  juggler's  knife, 
in  the  attempt  to  swallow  it,  was  arrested  in  the  oesopha- 
gus and  wore  a  way  into  the  pericardium ;  and  that  re- 
ported by  McDowel,  in  which  a  cavity  of  the  left  lung 
had  penetrated  the  pericardium. 

The  Signs  of  Pneumo-pericardium. — The  few  physicians 
who  have  reported  cases  of  pneumatosis  of  the  pericardium 
are  entirely  agreed  regarding  the  diagnostic  signs.  It 
appears  that  no  case  has  been  yet  recognized  of  air  or  gas 


94  PERICARDITIS. 

in  this  cavity  in  which  there  was  not  fluid  of  some  kind  in 
it  at  the  same  time,  and  hence  the  most  characteristic 
feature  of  the  case — the  churning,  or  splashing,  or  water- 
wheel  sound.  This  is  heard  in  systole,  and  with  every 
contraction.  In  some  this  sound  has  been  heard  at  some 
distance  from  the  body,  in  others  only  by  actual  applica- 
tion of  the  ear  to  the  praecordial  space  ;  but  in  all  it  was 
distinct  and  unmistakable.  It  has  been  called  tympan- 
itic. Stokes  denominates  it  bruit  de  pot  feU^  Laennec, 
bruit  de  fluctuation. 

In  all  there  has  been  resonance  on  percussion  over  the 
heart,  which  changed  place  with  changed  position  of 
body. 

Dr.  G.  Tilling  reports  a  case  of  traumatic  haemato- 
pericardium.  The  patient  was  caught  between  two 
wagons ;  was  at  first  insensible,  but  recovered  con- 
sciousness and  walked  home.  He  was  spitting  blood 
when  first  seen,  twenty-four  hours  after  the  accident. 
The  apex-beat  of  the  heart  was  perceived  by  the  eye,  dif- 
ficult to  feel,  and  diffused.  The  area  of  dulness  extended 
a  finger's  width  beyond  the  right  edge  of  the  sternum. 
The  heart  sounds  were  marked  by  various  indescribable 
murmurs  in  this  region,  but  were  clear  and  distinct  at  the 
second  intercostal  space,  no  air  in  either  pleura  or  peri- 
cardium, no  fracture,  pulse  slow,  54  to  'J^.  Was  the  di- 
agnosis of  hsemo-pericardium,  as  against  hydro-pericar- 
dium sustained  by  the  facts  as  reported  ?  The  patient 
recovered.     (The  Medical  Record,  Sept.  23,  1882.) 

Dr.  Tilling  thinks  that  the  following  symptoms  justify 
him  in  believing  that  there  was  an  effusion  of  blood  into 
the  pericardium  in  this  case  of  injury  of  the  chest  which 
did  not  break  any  ribs.  Cardiac  dulness  extended  over 
the  right  border  of  the  sternum.  The  apex-beat  could 
only  just  be  felt,  but  could  not  be  located.  The  heart 
sounds  were  marked  by  a  variety  of  sounds,  blowing,  rub- 


PERICARDITIS.  95 

bi'ng,  and  splashing,  except  in  the  second  intercostal 
space,  where  they  were  clear.  The  peculiar  splashing 
sound  would  seem  to  indicate  a  "  partial  "  pneumo-peri- 
cardium.  A  similar  sound,  he  says,  was  recorded  by 
Morel  Lavallee  in  a  case  of  actual  haemato-pericardium,  as 
proven  on  inspection.  But  Tilling's  patient  recovered. 
On  the  third  day  the  rubbing  and  splashing  sounds  dis- 
appeared. In  a  case  reported  by  Billroth  he  SBys,  peri- 
carditis occurred  from  a  blow,  but  \:\\.^  presence  of  hcemato- 
pericardium  is  not  mentioned. 


96  ENDOCARDITIS. 


LECTURE   III. 

ENDOCARDITIS. 

In  my  opening  remarks  on  pericarditis  I  gave  you  the 
boundaries  of  dulness  produced  by  a  healthy  heart,  that 
you  might  know  when,  by  pericardial  effusion  or  other 
cause,  those  limits  were  exceeded.  So  now,  as  we  begin 
the  study  of  endocarditis  it  may  be  interesting,  and  per- 
haps more  interesting  than  useful,  to  state  to  you  the  exact 
position  of  the  four  valves  of  the  heart,  their  relative  po- 
sition,  and  their  relation  to  the  walls  of  the  chest.  This 
information  will  be  clinically  important  so  far  as  it  relates 
to  the  aortic  and  pulmonary  valves  ;  but  in  the  case  of 
both  auriculo-ventricular  valves  it  is  of  less  practical 
value,  because  the  sounds  produced  in  them  are  not 
heard  directly  over  them,  but  over  the  part  of  the  heart 
to  which  the  vibrations  are  conducted  by  the  apertures 
of  the  valve.  Yet  even  in  regard  to  them  it  cannot  be 
regarded  as  useless  knowledge. 

After  the  paper  on  "Auscultatory  Percussion,"  already 
referred  to,  was  prepared  and  had  been  sent  to  the  printer, 
I  began  (June  27,  1840),  in  association  with  the  late  Dr. 
Swett,  the  studies  to  be  here  reported.  A  careful  record 
was  made  at  the  time  of  what  we  did,  which  has  never 
been  published.  Indeed,  I  have  never  seen  a  report  of 
any  similar  experiments  by  anybody.  We  repeated  the 
trials  on  different  bodies  till  we  were  assured  that  the 
results  were  fairly  reliable,  choosing  those  in  which  there 
was  during  life  no  evidence  of  cardiac  disease. 

We  used  the  same  kind  of  penetrating  instruments 
that  were  used  in  defining  the  limits  of  the  heart,  i.e., 


ENDOCARDITIS.  97 

sharpened  steel  knitting-needles.  The  first  step  was  to 
raise  the  trachea  and  cut  it  just  below  the  cricoid  carti- 
lage, introduce  a  compressed  cork,  and  tie  the  cork  firmly 
in.  The  object  of  this  was  to  preserve  the  relations  of  the 
heart  and  lungs  by  preventing  the  escape  of  air  from  the  lat- 
ter, when  the  chest  should  be  opened  ;  and  also  to  prevent 
any  possible  change  in  the  position  of  the  heart  from  the 
same  cause.  Then  we  lAid  bare  the  sternum,  cartilages 
of  the  ribs,  and  part  of  the  ribs  in  the  praecordial  region. 

A  needle  was  forced  through  the  sternum  one  line  to  the 
right  of  the  median  line  of  the  body,  and  half  an  inch 
below  the  line  that  would  unite  the  points  when  the  lower 
edge  of  the  cartilages  of  the  third  ribs  join  the  sternum. 
The  needle  was  introduced  at  right  angles  to  the  plane 
of  the  body.  It  was  found  to  have  passed  just  outside 
the  aorta  to  the  right  on  the  level  of  the  free  border  of 
its  valve.  This  trial,  then,  states  that  the  whole  aortic 
valve  is  below  the  inferior  edge  of  the  third  rib  at  the 
sternum,  half  an  inch,, and  that  it  does  not  extend  more 
than  half  a  line,  or  the  twenty  fourth  of  an  inch  to  the 
right  of  the  middle  of  the  sternum. 

A  needle  introduced  at  the  same  point  in  another  body 
passed  into  the  top  of  the  right  ventricle,  barely  escaping 
the  ventricular  septum,  and  on  to  the  right  of  the  aorta,  and, 
entering  the  right  auricle,  touched  the  left  attachment  of 
the  tricuspid  valve.  A  little  deeper  it  passed  less  than  a 
line  to  the  right  of  the  right  limit  of  the  mitral  opening. 
Here,  then,  it  is  shown  that  the  aorta  at  its  origin  is  on 
the  left  of  the  point  chosen,  i.e.,  half  an  inch  below  the 
third  rib  and  one  line  to  the  right  of  the  middle  of  the 
sternum  ;  and  that  this  point  indicates  almost  exactly,  if 
we  measure  from  left  to  right,  the  end  of  the  mitral  open- 
ing, and  the  beginning  of  the  triscuspid,  of  course  on 
different  planes. 
A  needle  introduced  in  the  third  left  intercostal  space, 


gS  ENDOCARDITIS. 

equidistant  from  the  third  and  fourth  ribs,  and  in  contact 
with  the  sternum,  penetrated  the  posterior  aortic  cusp 
midway  between  its  free  border  and  its  attachment,  also 
at  a  central  point  from  right  to  left.  The  same  needle 
penetrated  the  anterior  curtain  of  the  mitral  valve,  passed 
through  this  opening  half  an  inch  from  its  right  extrem- 
ity. In  one  trial  the  needle  introduced  at  the  same  point 
left  the  middle  of  the  base  or  attachment  of  the  aortic 
valve  five  lines  above  it,  but  it  pierced  the  curtain  of  the 
mitral  valve  and  passed  through  the  opening  at  the  cen- 
tral point,  leaving  eight  and  a  half  lines  on  either  side  of 
it.  This  heart  was  that  of  a  man  who  died  of  typhoid 
fever,  and  the  heart  was  in  the  wet-rag  condition  of  Louis, 
everything  "  flattened  out."  Thus  it  appears  that  the 
aortic  and  mitral  valves  are  in  the  same  vertical  plane  ; 
commonly  in  the  same  horizontal  plane,  but  not  always 
— the  aortic  directly  in  front  of  the  mitral,  but  sometimes 
above  it. 

A  needle  penetrating  the  stern'i^m  at  a  point  one  line 
to  the  right  of  its  middle  and  one  inch  five  lines  below  the 
junction  of  the  third  rib  and  sternum,  lower  edge,  passed 
into  the  right  ventricle,  and  penetrated  the  tricuspid  cur- 
tain just  at  its  attachment,  and  midway  between  its  ex- 
tremities, entering  the  muscular  tissue  that  forms  the 
lower,  or  better,  the  right  lip  of  this  opening. 

The  pulmonary  valve  we  found  situated  further  to  the 
left  than  the  aortic,  and  only  a  line  above  it.  Measuring 
from  the  needle  that  was  inserted  in  the  middle  of  the 
intercostal  against  the  left  edge  of  the  sternum,  we  often- 
est  found  the  middle  of  the  base  of  the  aortic  valve  five 
lines  vertically  inward  ;  while  the  middle  of  the  base  of 
the  pulmonary  valve  was  six  lines  to  the  left  and  then 
six  lines  vertically  upward  measuring  still  from  the  same 
needle. 

From  these  trials  it  appears  that  the  aortic  valve  is 


ENDOCARDITIS.  00 

half  of  it  under  the  sternum  and  half  of  it  under  the 
lower  part  of  the  left  third  rib — that  the  pulmonary 
valve  is  almost  wholly  under  this  rib,  leaving  only  about 
a  line  of  its  width  under  the  sternum — that  the  mitral 
opening  begins  half  an  inch  below  the  lower  edge  of  the 
third  rib  at  the  middle  of  the  sternum,  and  extends  to 
the  left  and  a  little  upward  to  the  cartilage  of  the  third, 
in  a  state  of  collapse  eight  and  a  half  lines  from  the  left 
edge  of  the  sternum — and  that  the  tricuspid  begins  at  a 
point  less  than  a  line  to  the  right  of  the  right  limit  of  the 
mitral,  and  extends  almost  directly  downward,  being 
wholly  under  the  right  half  of  the  sternum. 

The  measurement  of  the  mitral  opening,  as  just  given, 
corresponds  to  a  circumference  of  thirty-four  lines,  and 
this  to  a  diameter  of  eleven  and  one  third  lines  when 
rounded  and  in  action.  This  would  diminish  the  lateral 
space  occupied  by  this  opening  from  seventeen  lines  to 
about  an  inch.  This  measurement  was  recorded  only  for 
the  purpose  of  saying  that  the  needle  was  at  the  exact 
middle  of  the  opening.  The  measure  of  the  other  orifices 
was  not  taken,  as  the  object  of  these  trials  was  to  ascer- 
tain position,  not  capacity. 

Knowledge  is  always  worth  having,  but  as  I  have  al- 
ready said  it  is  more  practically  important  to  know  the 
location  of  the  aortic  and  pulmonary  valves  than  that  of 
the  auriculo-ventricular.  In  case  of  the  first  we  listen 
directly  over  and  not  far  from  them  for  the  evidence  of 
unhealthy  changes  in  them,  but  the  indications  of  such 
changes  in  the  mitral  valve  are  often  not  obtainable  when 
the  ear  is  applied  exactly  in  front  of  it,  for  the  aortic  and 
pulmonary  artery  are  between  the  surface  and  the  valve, 
and  more  than  half  the  time  there  is  blood  in  the  ventri- 
cle coming  between  the  valve  and  the  ear  in  addition. 
But  this  valve  is  connected  with  the  walls  of  the  heart  by 
its  own  tissues,  and  by  the  tendinous  cords  and  fleshy 


too  ENDOCARDITIS. 

columns,  which  are  good  conductors  of  sound.  We  there- 
fore get  the  sounds  produced  here  most  clearly  over  a 
point  where  an  anterior  fleshy  column  is  incorporated 
with  the  cardiac  walls.  This  is  not  at  the  apex  exactly, 
but  about  three  quarters  of  an  inch  nearer  the  base,  but 
for  convenience  of  expression  and  shortness  we  almost 
always  call  it  '*  listening  at  the  apex." 

In  the  tricuspid  valve  the  anatomical  arrangements  are 
very  similar,  but  we  can  listen  over  it  with  better  chances 
of  perceiving  morbid  sounds,  because  the  right  ventricle 
is  superficial,  but  we  also  listen  just  off  the  sternum  in 
the  fourth  right  intercostal  space. 

Dr.  N.  Werp*  reports  an  instance  of  constant  diastolic 
murmur  for  four  weeks  before  death.  On  inspection 
there  was  found  a  patch  of  recent  endocarditis  on  the 
auricular  surface  of  the  aortic  half  of  the  bicuspid  (mitral) 
valve.  There  were  also  traces  of  old  endocarditis  at  the 
bicuspid  with  consecutive  valvular  aneurism,  endarter- 
itis deformans  of  the  aorta  with  dilatation  of  its  ascend- 
ing portion,  excessive  hypertrophy  of  the  left  ventricle, 
commencing  pericarditis.  The  little  aneurismal  pouches 
on  the  mitral  valve  were  turned  with  their  cups  facing  the 
auricle,  and  were  also  slightly  roughened.  There  was  no 
stenosis  of  the  venous  opening  into  the  auricle.  Here, 
then,  there  was  no  valvular  lesion  (?)  in  the  ordinary  clini- 
cal sense  of  the  term,  yet  there  was  a  persistent  diastolic 
murmur  at  the  mitral  opening. 

Now  we  are  ready  to  pursue  our  study  of  endocarditis. 
I  have  gone  into  this  explanation  of  the  action  of  the 
valves,  and  the  effects  of  their  not  working  properly  be- 
cause endocarditis  is  a  deformer  of  valves. 

When  inflammation  occurs  in  the  endocardium,  we  are 
not  sure  that  it  affects  the  whole  extent  of  the  endocar- 

*  The  Med.  Record,  Sept.  23,  1883. 


ENDOCARDITIS.  lOI 

dial  membrane.  We  are  sure  that  it  occurs  about  the 
valves.  The  tendency  of  persons  who  write  about  dis- 
eases of  the  heart  is  to  confine  the  inflammatory  action  to 
the  valves.  Now,  it  is  not  necessary  that  the  inflamma- 
tory action  should 'be  confined  to  the  valves  even  from 
what  we  see.  If  there  is  an  exudation  upon  the  border 
of  the  ventricle,  for  example,  on  that  part  of  the  endo- 
cardium, it  will  be  washed  off  by  the  current  of  blood 
that  is  continually  flowing,  and  flowing  with  a  good  deal 
of  force,  through 'the  heart.  You  ask  why  it  would  not 
be  washed  off  from  the  valves  ?  Because  it  holds  fast 
there.  The  effusion  is  between  the  folds  that  make  the 
curtains  of  this  valve  on  the  attached  surface  of  these 
folds,  and  it  cannot  readily  get  out.  Then  there  is  a 
form  of  inflammation  called  ulcerative  endocarditis  that 
attacks  any  portion  of  the  endocardium.  I  will  explain 
that  further  on.  The  point,  then,  I  make  is,  that  be- 
cause the  results  of  the  inflammation  are  found  only  in 
and  about  the  valves,  it  does  not  follow  that  the  whole 
endocardium  may  not  have  been  the  seat  of  disease. 

The  question  occurs,  what  changes  take  place  in  the 
endocardium  during  the  inflammatory  process?  I  do  not 
know  whether  it  becomes  red,  except  by  analogy.  No- 
body has  ever  seen  the  endocardium  at  the  commence- 
ment of  endocarditis.  We  cannot  say,  then,  that  we 
know  the  membrane  is  red.  We  can  infer  that  it  is 
probable,  because  membranes  that  are  inflamed  anywhere 
else,  so  far  as  we  know,  are  red  at  the  beginning  of  the 
inflammatory  process,  becoming  less  and  less  red  as  the 
inflammation  exhausts  itself.  Roughnesses  are  not  com- 
monly made  (except  in  particular  kinds  of  inflammation) 
upon  the  body  of  the  endocardium,  but  here  at  the  valves. 
You  may  expect  from  endocarditis,  first,  a  thickening  of 
the  valves ;  and  second,  a  growth,  either  upon  the  valves 
or  near  them   (but   this  is   not   constant)  of   little   emi- 


I02  ENDOCARDITIS. 

nences,  little  granulations,  you  might  call  them,  which 
are  described  as  being  firm  at  the  base,  and  by  microscop- 
ical examination  found  to  be  composed  of  connective  tis- 
sue at  the  base,  but  of  new  and  soft  cells  at  the  top,  so 
that  the  base  of  these  little  granulations  is  firmer  than  the 
apex.  One  of  the  most  important  facts,  perhaps,  in  the 
whole  history  of  endocarditis  is  the  formation  of  little 
granulations  upon  these  valves,  causing  the  blood  to 
precipitate  its  fibrine  upon  these  rough  surfaces.  You 
are,  perhaps,  aware  that  if,  in  an  animal,  a  thread  be  run 
through  a  vein  or  artery  so  as  to  pierce  it  about  its  mid- 
dle, the  fibrine  will  collect  upon  that  thread  and  form  a 
clot,  a  considerable  little  ball ;  or  it  will  be  swept  in  the 
direction  of  the  circulation.  Any  rough  body  in  an  ar- 
tery, or  in  the  heart,  or  in  a  vein,  will  cause  a  coagula- 
tion of  blood  about  it,  the  fibrinous  portion  of  blood 
making  the  clot.  Well,  here  this  roughened  surface  has 
become  encrusted,  so  to  speak,  or  covered  by  a  coagula- 
tion of  fibrine,  having  some  blood-coloring  matter  in  it  to 
give  it  a  red  color.  Now,  this  is  the  worst  thing  that  can 
happen  in  endocarditis,  for  the  reason  that  these  concre- 
tions, these  aggregations  upon  any  rough  surface  of  the 
heart,  are  apt  to  be  washed  away  and  carried  into  the 
organs  of  the  body — into  the  brain,  not  infrequently ; 
rarely  into  the  liver,  because  the  liver  circulation  from 
the  heart  direct  is  feeble,  being  supplied  chiefly  by  the 
portal  circulation.  But  the  brain  lesions  are  the  worst, 
and  this  embolism  carried  from  the  heart  valves  most  fre- 
quently, or  from  any  portion  of  the  heart,  to  the  arteries 
of  the  brain,  will  frequently  produce  apoplexy — of  course, 
a  pretty  grave  matter.  The  principal  points  to  be  noted 
with  reference  to  the  effect  of  endocarditis  are :  first, 
thickening  of  the  valves  by  an  effusion  between  their 
folds ;  and,  second,  these  granulations  growing  up  in  dif- 
ferent parts  of  the  endocardium,  mostly  upon  the  valves 


ENDOCARDITIS.  IO3 

which  have  lain  traps  and  caused  a  deposit  of  the  fibrine 
of  the  blood  upon  them,  making  what  we  usually  call 
vegetations,  and  these  are  constantly  apt  to  be  washed 
off  and  carried  into  important  parts  of  the  body  and  do 
serious  harm. 

Now,  the  material  that  produces  thickening  of  these 
valves  is  not  exactly  like  ordinary  false  membrane.  The 
inspection  of  it  by  the*  microscope,  when  it  is  recent, 
shows  that  it  is  a  transparent,  opaquish  fluid,  filled  with 
new  cells,  not  of  the  kind  that  we  refer  to  pus,  but  those 
that  are  capable  of  combining  and  being  propagated  into 
fibrine.  The  false  membrane  met  with  in  endocarditis 
is  made  in  a  different  way  from  ordinary  false  membrane, 
with  which  you  have  already  become  somewhat  familiar. 
It  has  no  property  of  its  own.  It  is  coagulated  into 
fibres  by  the  addition  of  acetic  acid ;  at  least,  Virchow 
says  so,  and  he  compares  it  with  mucine. 

This  product  may,  at  first,  swell  the  valve  considerably, 
and  afterward  contract  by  the  absorption  of  its  fluid  part, 
and  then  it  may  become  organized  with  the  two  folds  of 
the  valves.  The  result  of  this  will  be  a  thickened  and 
clumsy  valve.  And  as  this  new  material  contracts  it  con- 
tracts the  valve,  the  valve  is  shortened  so  that  it  cannot 
reach  its  fellow  in  the  middle  of  the  artery,  and  it  is  very 
much  stiffened  and  hardened  ;  it  is  of  the  consistency  of 
leather  sometimes.  The  defect  described  is  the  cardinal 
one.  The  valves  are  thickened,  they  are  shortened,  they 
are  stiffened,  they  cannot  perform  their  office.  The  result 
of  this  is  obstruction,  and  again,  regurgitation,  one  or 
both,  as  may  occur  in  a  particular  case. 

Now,  then,  with  reference  to  the  recognition  of  these 
changes  as  they  are  coming  on.  You  sometimes  can 
recognize  them  and  sometimes  cannot.  Endocarditis  is 
very  apt  to  occur  with  pericarditis,  and  it  is  often  difficult 
to  determine  whether  there  is  endocarditis  or  not. 


I04  ENDOCARDITIS. 

There  may  be  a  grade  of  inflammation  of  the  endo- 
cardium and  of  the  valves  that  will  not  produce  this 
mucine  matter,  but  merely  oedema.  The  valves  may  be- 
come thickened  by  becoming  bags  of  water.  Now  this 
is  a  form  of  disease  that  is  sometimes  recognized,  but  not 
by  the  rational  signs.  To  recognize  an  endocarditis  by 
rational  signs  is  impossible,  and  perhaps  this  is  a  good 
reason  why  it  was  not  recognized  during  life  till  ausculta- 
tion became  an  art,  and  endocarditis  may,  in  that  sense, 
be  called  the  child  of  auscultation.  When  this  oedema- 
tous  effusion  occurs,  the  valves  are  obstacles  to  the  free 
flow  of  the  blood,  and  produce  a  murmur.  If,  then,  you 
have  listened  at  a  particular  time  to  the  heart  and  found 
no  murmur  of  any  kind,  and  you  have  symptoms  of  a  very 
vague  kind,  and  you  suspect  endocarditis,  if  you  listen 
again  you  may  possibly  hear  an  endocardial  murmur,  and 
it  is  very  likely  to  be  at  the  aortic  opening. 

Relating  to  endocarditis,  the  matter  of  vegetation, 
commonly  so  called  in  this  country,  is  of  interest.  I  told 
you  that  endocarditis  is  sometimes  attended  by  the  for- 
mation of  little  granulations  growing  out  of  the  endocar- 
dium, firm  at  the  base  and  soft  at  the  top,  not  so  large  as 
a  pin's  head  ;  and  that  these,  though  of  very  diminutive 
size,  are  capable  of  being  the  nucleus  around  which 
the  fibrine  of  the  blood  will  coagulate,  or  rather  will  be 
gathered,  and  become  of  visible  form.  What  we  call 
vegetation,  the  German  writers  regard  as  an  accretion, 
but  we  are  both  correct  in  regard  to  its  nature,  viz.,  that 
it  is  substantially  the  fibrine  separated  from  the  blood  in 
the  same  way  as  it  is  separated  when  a  thread  is  run 
through  an  artery  or  vein.  Any  cause  that  produces 
roughness,  as  an  ulcer  or  any  irregularity,  is  liable  to  be 
surrounded  by  this  accretion  of  fibrine.  While  we  rarely 
see  a  membranous  exudation  in  endocarditis  upon  the 
body  of  the  heart,  on  its 'inner  surface,  that  can  be  easily 


ENDOCARDITIS.  I05 

accounted  for,  under  the  supposition  that  the  exu- 
dation has  thickened  and  fallen  off  by  the  continual 
■\yashing  of  the  surface  by  the  current  of  blood.  In 
this  specimen  you  see  some  deposit  of  fibrine  on  the 
three  aortic  curtains.  And  here  is  that  rather  inter- 
esting— I  don't  know  but  I  ought  to  say  ornamental — 
formation  of  granules,  forming  a  semicircle  on  the  free 
portions  of  the  valves.  This,  however,  illustrates  athe- 
roma. 

One  of  the  dangers,  as  I  have  said,  of  endocarditis  is 
the  washing  away  of  these  deposits  into  the  general  circu- 
lation, and,  finally,  the  lodgment  of  a  mass  of  this  kind  in 
an  artery,  through  which  it  cannot  pass.  Endocarditis  of 
itself  is  almost  never  fatal.  It  accompanies  pericarditis  in 
a  great  majority  of  cases  of  pericarditis,  and  for  the  most 
part,  when  so  associated,  depends  upon  the  same  cause. 
Yet  endocarditis  can  occur  even  in  the  acute  form,  and 
frequently  it  does  occur  in  the  chronic  form,  without  any 
rheumatism  preceding  it,  without  any  of  the  diseases  that 
are  apt  to  be  associated  with  pericarditis,  as  Bright *s  dis- 
ease, scarlet  fever,  purulent  inflammation  of  the  body, 
septicaemia.  I  have  sometimes,  by  exclusion,  been  able 
to  say  that  a  certain  person  has  endocarditis.  I  form 
such  an  opinion  when  I  find  a  certain  amount  of  febrile 
action,  a  little  elevation  of  temperature,  a  little  increased 
frequency  of  the  breathing,  and  a  short,  irritable,  quick- 
ened beat  of  the  heart.  That  short,  irritable  beat  will 
produce  in  the  ear  the  same  sound  that  I  referred  to  in 
describing  pericarditis  ;  when  it  was  first  noticed  it  was 
regarded  as  diagnostic,  but  it  has  no  such  value.  It  is 
just  that  metallic  ring  which  you  get  by  applying  the 
palm  of  the  hand  to  the  ear  to  exclude  the  air,  and  then 
striking  on  the  back  of  it.  It  is  the  irritable  beat  of  the 
heart  against  the  inner  wall  of  the  chest  that  produces  it. 
You  should  be  able  to  exclude  everything  that  would  be 


Io6      ^       ,  ENDOCARDITIS. 

likely  to  produce  a  febrile  movement,  and  perhaps  you 
may,  in  half  the  cases,  find  that  the  diagnosis  of  endocar- 
ditis is  verified  by  after  indications.  During  the  progress 
of  endocarditis  there  are  frequently  no  indications  of  its 
presence  except  pericarditis.  You  assume,  usually,  at 
once,  when  you  diagnose  acute  pericarditis,  that  there  is 
endocarditis,  but  of  itself  it  does  not  give  distinctive 
signs  except  in  a  few  cases.  When,  for  example,  you 
have,  say  rheumatism,  or  Bright's  disease,  and  have  lis- 
tened to  the  heart  on  a  certain  day  and  have  found  noth- 
ing unnatural,  you  find  the  illness  is  increased  a  little,  the 
heart  beating  more  frequently,  the  respiration  short  and 
frequent,  you  listen  again  and  you  get  an  endocardial 
murmur.  It  is  probably  soft.  It  may  be  at  the  aortic 
opening  ;  it  may  be  at  the  mitral.  Supposing  it  to  be  in 
the  interval  of  the  heart's  action,  during  the  period  of  re- 
pose, it  is  produced  by  one  of  two  things :  an  cedema- 
tous  valve,  or  the  little  granulations  I  have  been  describ- 
ing forming  upon  the  surface  that  the  blood  has  to  pass 
over.  In  a  few  instances  you  may  get  that  aid  to  diag- 
nosis, but  in  the  majority  you  do  not.  Then,  again, 
there  may  be  an  cedematous  swelling  of  the  aortic  valve  ; 
the  two  folds  that  constitute  the  valve  are  swelled  out 
and  partly  fill  the  passage  through  which  the  blood  should 
flow.  A  soft  murmur  is  sometimes  produced  in  that  case, 
but  as  it  is  only  sometimes  it  cannot  be  relied  on  as  a 
diagnostic  mark,  except  when  you  have  listened  a  few 
days  before  and  found  no  murmur,  and  now,  with  indica- 
tions that  there  may  be  endocarditis,  you  do  find  one, 
then  it  is  sufficient ;  but,  in  practice,  neither  the  rational 
nor  the  physical  signs  of  endocarditis  are  sufficiently 
marked  to  enable  anybody  to  make  a  certain  diagnosis 
without  one  of  these  facts  that  I  have  just  now  referred  to. 
In  general,  endocarditis  comes  during  its  acute  period 
without  producing  any  symptom,  only  that  short  irritable 


ENDOCARDITIS.  I07 

beat  of  the  heart  and  the  increase  in  the  frequency  of  the 
respiration.  The  rational  diagnosis  is  entirely  vague. 
The  physical  diagnosis  also  is  very  uncertain.  But  the 
after  diagnosis  is  less  difficult — you  may  lock  the  door 
after  the  horse  is  stolen — the  after  diagnosis  is  certain. 
The  deposit  in  these  valves,  if  it  is  anything  more  than 
oedema,  is  pretty  sure  to  produce  changes  in  the  struc- 
ture of  the  valves.  In 'the  first  place,  they  must  be 
thickened,  for  there  is  new  rnatter  deposited  in  their 
structure ;  in  the  second  place,  this  new  matter  under- 
goes organization.  It  behaves  like  a  false  membrane, 
and  shortens,  and  the  valve  is  shortened,  so  that  when  it 
atternpts  to  fill  the  opening  that  it  is  appointed  to  fill  it 
cannot.  There  is  a  hole  left  in  the  middle.  The  valve 
may  sometimes  grow  hard  and  stiff,  like  leather,  and  then 
can  do  very  little  in  preventing  the  return  of  blood,  but 
a  good  deal  in  preventing  the  outflow  of  blood.  When 
these  changes  occur,  even  in  a  moderate  degree,  you  will 
get  a  murmur.  It  will  very  likely  be  of  a  harsh  kind.  It 
is  not  however  certain  to  be  that  at  first.  It  will  grow  to 
be  a  harsh  murmur,  in  all  probability,  in  a  few  months. 
The  period  of  time,  however,  at  which  you  can  recognize 
the  murmurs  will  be  from  three  weeks  to  three  months 
after  the  disease  has  passed,  after  the  time  when  your 
diagnosis  would  be  of  any  practical  value.  But  the  thing 
stands  so.  You  have  to  take  it  as  it  is.  You  can  pretty 
safely  say,  after  two  or  three  months,  this  patient  has  had 
endocarditis.  But  as  it  is  so  frequently  associated  with 
pericarditis,  and  as  pericarditis  is  easy  of  recognition, 
and  as,  further,  the  treatment  of  the  one  condition  is  the 
same  as  the  treatment  of  the  other  when  they  are  asso- 
ciated, this  lack  of  power  of  diagnosis  is  not  disastrous. 
It  is  only  important  when  the  disease  occurs  alone ;  and 
that  it  does  occur  alone  we  have  pretty  good  evidence  in 
the  great  number  of  persons  that  we  see  with  valvular 


I08  '        ENDOCARDITIS.        ^^     . 

disease  who  have  never  had  rheumatism,  never  had 
Bright's  disease,  never  had  any  of  the  affections  that  are 
so  apt  to  precede  pericarditis  and  endocarditis.  They 
have  enjoyed,  as  they  believe,  good  health,  and  cannot 
point  to  any  time  when  they  have  had  symptoms  that 
would  lead  us  to  think  that  they  had  had  heart  disease; 
yet  the  valves  have  become  thickened  and  are  defective, 
just  as  they  are  in  the  acute  form  of  the  disease.  There 
is  then  undoubtedly  a  chronic  endocarditis,  that  only 
shows  itself  by  the  physical  changes  that  are  produced, 
or  rather  by  the  changes  that  are  produced  in  the  sounds 
of  the  heart.  Dr.  A.  J.  Harrison,"^  after  detailing  three 
cases  of  endocarditis,  occurring  without  disease  of  the 
joints,  urges  that  the  occurrence  of  the  disease  in  this  way 
as  a  primary  affection  is  not  very  rare,  especially  in  those 
predisposed  to  rheumatism.  He  is  inclined  to  regard 
endocarditis  as  one  of  the  regular  symptoms,  rather  than 
one  of  the  frequent  sequelae  of  rheumatic  fever.  Haskins 
believes  that  the  disease  is  actually  the  initial  fact  in 
every  attack  of  rheumatism,  and  that  its  presence  can 
always  be  substantiated  by  physical  signs.  Others,  while 
acknowledging  the  constancy  of  roughened  heart  sounds 
in  rheumatism,  do  not  consider  that  this  sign  possesses 
the  significance  Dr.  Haskins  assigns  to  it. 

Dr.  Harrison  also  read  before  the  British  Medical  Asso- 
ciation *  the  history  of  four  cases  of  primary  endocarditis. 
The  president,  Dr.  Allbutt,  said  that  cardiac  disease 
should  not  be  taken  as  a  test  of  severity  of  rheumatic 
fever.  Endocarditis  was  frequently  the  first  event  in  that 
fever.  It  is  not  uncommonly  the  only  event.  He  referred 
to  cases,  and  especially  to  one  in  which  endocarditis  oc- 
curred without  other  local  manifestations. 

Dr.  'Balfour  said  that  every  case  of  systolic   murmur 

*N.  Y.  Med.  Jour.,  March,  3,  1883. 
*The  Medical  Record,  Aug.  26,  1883. 


ENDOCARDITIS.  10^ 

should  not  be  considered  a  case  of  endocarditis,  because 
a  certain  amount  of  rheumatism  might  occur  without 
any  endocarditis;  then  he  had  not  seen  a  case  of  rheuma- 
tic fever  in  which  there  was  not  a  systoHc  murmur.  In 
fever  of  all  kinds,  especially  in  feeble  persons,  a  systolic 
murmur  could  almost  invariably  be  detected.  Besides  he 
thought  that  every  case  of  friction  should  not  be  regarded 
as  a  case  of  pericarditis. 

Dr.  Ashley  remarked  that  he  had  frequently  observed 
endocardial  and  pericardial  murmurs  in  connection  with 
slight  attacks  of  tonsillitis.  A  fact  long  ago  observed 
was  that  tonsillitis  had  a  casual  connection  with  rheu- 
matic fever,  the  same  as  influenza. 

The  relation  of  these  changes  to  the  structure  of  the 
heart  itself  will  be  for  consideration  hereafter.  You  ob- 
serve, then,  you  have  not  a  very  certain  diagnosis.  Only 
when  you  have  listened  and  heard  no  endocardial  mur- 
mur, and  then,  a  few  days  after,  with  symptoms  of  ill-, 
ness,  do  find  one,  are  you  enabled  to  make  a  diagnosis. 
And  then  you  have  to  be  certain  that  it  is  an  endocar- 
dial,— not  an  exocardial  murmur.  The  statement  I  have 
made  with  reference  to  the  breathing  will  aid  you  in  mak- 
ing the  diagnosis. 

Dr.  Putnam-Jacobi  *  reported  to  the  N.  Y.  Pathologi- 
cal Society  the  case  of  a  child  thirteen  years  of  age  who 
gave  proofs  of  a  prior  attack  of  both  left  and  right  endo- 
carditis, which  probably  occurred  during  an  attack  of 
rheumatism  a  year  before  her  death,  and  also  deposits  by 
an  endocarditis  of  the  right  side  that  were  recent  fibrine 
particles  from  the  last  deposits  which  had  been  swept  into 
the  pulmonary  current  and  produced  embolism,  and  in  turn 
she  thinks  produced  pneumonia,  and  this  again  pleurisy, 


*  The  Medical  Record,  March  17,  1883. 


no  ENDOCARDITIS. 

4 

both  of  which  existed.  Colomeatte  *  describes  five  cases 
of  acute  endocarditis  of  the  tricuspid  valve,  and  says  that 
this  inflammation  may  fall  on  the  tricuspid  or  sigmoid 
valve  alone,  or  on  both  at  the  same  time  ;  that  it  may  be 
perforating  at  one  orifice  while  it  causes  vegetations  at 
the  other.  It  is  found  in  infants,  in  youth,  in  old  age, 
and  in  both  sexes.  From  a  sixth  case  he  infers  that  endo- 
carditis may  affect  only  the  right  wall,  or  the  vegetations 
may  be  limited  to  the  right  auricular  appendage. 

These  vegetations  were  composed  of  embryonic  con- 
nective tissue,  the  elements  of  which  were  for  the  most 
part  in  a  state  of  fatty  degeneration.  They  were  easily 
torn  and  frequently  caused  pulmonary  emboli. 

Dr.  Ord,  St.  Thomas's  Hospital  Reports,f  relates  a 
case  in  which  shivering  fits  occurred  daily  for  a  fortnight, 
then  every  other  day,  and  then  every  thifd  day.  After 
admission  the  patient  had  daily  rigors  for  five  weeks, 
when  he  died.  There  was  on  admission  a  marked  presys- 
tolic thrill  over  the  impulse,  a  systolic  murmur  at  the 
apex  conducted  into  the  left  axilla,  and  a  fainter  and 
apparently  independent  systolic  murmur  over  the  aortic 
valve.  The  arteries  were  everywhere  much  thickened. 
The  liver  and  spleen  were  large,  and  the  spleen  was  tender 
for  one  week. 

At  the  post-mortem  examination  there  was  found  peri- 
cardial effusion  15  oz.,  but  no  lymph  ;  dilatation  of  both 
ventricles  and  hypertrophy  of  the  left.  The  posterior  set 
of  chordae  tendiniae  of  the  mitral  valve  were  ruptured, 
their  free  ends  clubbed  and  covered  with  black  clot.  The 
endocardium  showed  a  white  tract,  where  the  free  end 
would  have  played  against  it.  Bright*s  kidney,  large 
white;  large  liver. 


*The  Medical  Record,  Feb.  24,  1883,  from  "London  Medical  Record,  Jan. 
15,  18S3. 
\  Am.  Jour,  of  Med.  Science^  Oct.  1882. 


ENDOCARDITIS.  Ill 

Prof.  Leyden*  calls  attention  to  the  frequent  resem- 
blance of  the  temperature  curve  to  that  of  intermittent 
fevers.  This  fact  has  been  many  times  observed  by 
others.  He  makes  four  groups  of  cases  clinically.  The 
first,  those  cases  in  which  the  endocarditis  forms  part  of 
a  pyaemic  or  septic  process.  This  is  best  known  in  con- 
nection with  puerperal  septicaemia,  in  which  ulcerative 
(infectious  parasitic)  endocarditis  is  not  uncommon.  It  is 
also  met  with  sometimes  in  septicaemia  and  phlebitis 
following  injuries.  Leyden  observed  one  such  case  con- 
nected with  abscess  of  the  liver.  As  in  these  cases  the 
affection  is  general,  the  rigors  may  be  a  symptom  of  gen- 
eral sepsis,  quite  as  much  as  of  the  endocarditis.  In  the 
second  group  he  places  those  cases  which  are  marked  by 
a  more  or  less  intense  and  irregular  pyrexia  and  erratic 
rigors.  Traube.  and  others  have  recorded  such  cases. 
Volmer  had  a  case  in  which  typhoid  symptoms  appeared 
first,  then  rigors,  and  the  disease  was  recognized.  The 
third  and  fourth  groups  comprise  cases  in  which  the  tem- 
perature curve  corresponds  more  or  less  closely  to  that  of 
intermittent  fever,  with  periods  of  paroxysmal  exacer- 
bation alternating  with  apyrexia,  sometimes  for  a  short 
period,  regularly  quotidian  or  tertian  in  type.  In  the 
third  are  those  cases  in  which  the  signs  of  heart  disease 
are  ill-marked  and  null  till  near  the  close  of  life,  and  in  the 
fourth  those  in  which  heart  disease  has  been  long  estab- 
lished, the  intermittent  fever  occurring  as  a  final  compli- 
cation. He  details  four  such  cases.  This  disease  was  not 
known  to  physicians  of  the  last  century,  Morgagni,  for 
example. 

With  regard  to  the  treatment,  if  endocarditis  occur  in 
connection  with  rheumatism,  as  it  often  does,  the  treatment 
for  rheumatism  is  the  best  treatment  for  the  endocarditis, 


'^^  Medical  News,  June  24,  1882. 


112  '  ENDOCARDITIS. 

as  it  is  for  pericarditis.  If  you  can  recognize  the  disease 
as  occurring  alone,  then  I  would  advise  the  abstraction  of 
a  little  blood  ;  unload  the  vessels ;  relieve  the  valves  of  a 
part  of  their  work ;  not,  however,  more  than  eight  or  ten 
ounces.  You  will  be  tempted  to  apply  counter  irritation 
over  the  pericardial  region.  Well,  that  is  orthodox,  but 
it  is  useless.  There  is  no  way  of  affecting,  by  counter 
irritation,  the  circulation  in  the  endocardium.  It  is  en- 
tirely dependent  upon  the  coronary  arteries  of  the  heart, 
and  these  are  given  off  at  a  point  that  you  cannot  reach 
to  influence  the  amount  of  blood  circulating  in  them  by 
any  outside  application.  But,  if  it  will  satisfy  you  better, 
if  your  conscience  tells  you  the  patient  ought  to  have  a 
blister,  put  on  one  ;  though  it  will  prevent  your  listening 
so  satisfactorily,  it  will  do  no  harm,  and  I  don't  believe 
it  will  do  any  good.  In  quieting  the  heart's  irritation  a 
moderate  dose  of  opium  is  of  value.  The  more  quietly 
the  heart  can  do  its  work,  the  fewer  the  embarrassments, 
the  less  the  mischief  that  will  follow.  The  strain  upon 
the  valves,  whenever  they  are  brought  into  exercise,  is 
considerable — for  example,  that  against  the  mitral  when 
the  heart  is  contracted  ;  that  against  the  aortic  valves 
after  the  heart  is  contracted,  and  while  the  arteries  are 
contracted.  So  that  if  the  heart  does  its  work  in  the 
quietest  possible  way  the  mischief  to  these  valves  will  be 
the  least  that  you  can  expect.  Then  you  have  really  only 
two  things  that  are  of  much  consequence,  and  these  two 
are  the  abstraction  of  blood  and  quieting  the  heart  with 
opium  or  some  other  anesthetic. 

There  is  another  form  of  endocarditis  which  has  been 
lately  described,  or  within  a  few  years,  at  any  rate,  that 
you  will  not  be  able  to  recognize  at  all.  Still,  it  is  well 
enough  that  you  should  know  that  such  a  disease  exists. 
It  has  been  called  ulcerative  endocarditis.  It  seems  to 
be  a  sort  of  diphtheritic    inflammation.     A  diphtheritic 


BNDOCARDtTIS.  ll^ 

inflammation  of  a  mucous  membrane,  of  the  trachea,  for 
example,  or  the  fauces,  differs  from  a  common  croup  or 
other  membranous  inflammatory  action  in  the  fact  that 
the  deposition  that  is  the  result  of  inflammatory  action  is 
to  a  certain  extent  incorporated  with  the  membrane;  so 
to  speak,  infiltrated  into  it.  A  croupous  membrane  can 
form  and  can  exfoliate  and  leave  the  membrane  entirely. 
A  diphtheritic  membran^  can  exfoliate,  but  it  is  not  like- 
ly to  leave  the  membrane  perfectly  sound  and  normal. 
Sometimes  it  does,  but  it  is  the  tendency  of  diphtheritic 
inflammation  to  deposit  the  products  of  inflammatory 
action  in  the  tissue.  Well,  that  seems  to  occur  in  the 
endocardium,  and  it  may  occur  in  any  part  of  the  endo- 
cardium, not  alone  in  the  valves.  It  does  not  occur  so 
frequently  in  the  valves  as  on  the  body  of  the  endocar- 
dium. I  should  be  disposed  to  regard  it  as  a  sort 
of  diphtheritic  inflammation.  The  new  deposit  looks 
like  a  membranous  patch.  It  is  in  patches.  It  does 
not  extend  over  the  whole  surface,  and  when  you 
examine  it  post  mortem,  you  will  think  you  can  wipe 
it  off  with  your  scalpel,  or  with  a  rag,  but  when  you 
attempt  to  do  so  it  holds  fast,  and  if  you  with  your 
scalpel  attempt  to  remove  it  you  remove  the  membrane 
with  it.  This  proves  to  be  ulcerative  in  its  results.  It  is 
not  ulcerative  in  the  beginning.  It  is  simply  a  deposit  of 
diphtheritic  membrane  on  and  in  the  endocardium.  But 
it  has  not  the  power  to  perpetuate  its  life,  if  it  has  any, 
and  in  a  little  while  it  will  begin  to  break  down  into  fine 
granular  matter,  and  perhaps  some  oily  products,  and  as 
it  does  this  it  destroys  the  membrane  in  which  it  is 
deposited.  The  endocardium,  then,  is  susceptible  of 
destruction  in  limited  portions  of  its  extent  in  this  way. 
As  the  inflammatory  exudation  breaks  up  and  disappears 
it  carries  with  it  a  portion  of  the  endocardium.  If  that 
occurs  upon  the  valves,  as  it  sometimes  does,  it  is  very 


1 14  ENDOCARDITIS. 

likely  to  weaken  that  half  of  the  valve,  that  layer  or  fold 
of  the  valve,  so  much  that  aneurism  may  take  place  in 
this  valve.  That  is,  the  remaining  membrane,  the  mem- 
brane that  forms  the  other  half  of  the  valve,  will  not  bear 
the  strain  that  is  brought  upon  it  by  the  regular  course 
of  the  circulation,  and  it  pouches;  it  makes  a  bag,  or,  in 
other  words,  an  aneurism,  and  it  has  been  known  to 
rupture  under  these  circumstances.  Then,  again,  the 
ulcerative  process  may  not  be  confined  to  the  endo- 
cardium if  it  occurs  upon  the  body  of  the  heart.  It  may 
penetrate  a  little  distance  into  the  muscular  layers  and 
weaken  them,  and  hence,  also,  aneurism  of  the  heart  has 
occurred,  or  rupture  of  the  heart.  This,  as  I  have  told 
you,  is  a  form  of  inflammation,  or  a  product  of  inflamma- 
tion that  you  cannot  recognize  during  life.  It  produces 
no  physical  signs.  It  produces  no  peculiar  rational  signs. 
It  may  be  found  hereafter  that  it  is  confined  to  those  who 
have  some  diphtheria  in  other  parts  of  the  body.  And 
at  this  point  I  may  as  well  say  to  you  that  when  diph- 
theria made  its  appearance  in  New  York  for  the  first 
time  as  an  affection  of  the  throat  and  air  passages,  I  was 
interested  to  know  what  sort  of  thing  it  was,  and  I  early 
procured  specimens  of  the  membrane  for  microscopical 
examination.  I  found  that  it  was  made  of  granules  in 
great  degree — granules  that  were  held  together  by  a 
pretty  firm  matrix,  and  that  the  matrix  was  transparent ; 
that  on  the  outside  of  the  membrane,  that  is  on  the  side 
exposed  to  the  air,  there  were  the  common  microscopic 
vegetations,  two  or  three  forms  of  them.  And  that  in 
this  respect  the  diphtheritic  membranes  differed  from  the 
true  croupous  membranes,  being  constituted  in  very 
considerable  part  of  granules,  and  in  part  also  of 
extraneous  vegetations.  At  a  later  day  it  was  claimed 
that  these  granules  were  a  particular  vegetation  of  them- 
selves,  and   they   have   received   a   name  —  micrococci. 


ENDOCARDITIS.  1 1 5 

Micrococcus  iileails  a  little  berry.  These  bodies  are 
rounded,  and  in  these  membranes  are  packed  together 
pretty  closely.  As  you  read  the  journals  and  new  books 
you  see  a  good  deal  of  micrococcus.  It  seems  to  have 
found  its  way  into  parts  of  the  body  that  have  been 
supposed  before  to  be  sealed  to  any  outside  thing.  Well, 
they  tell  us  that  ulcerative  endocarditis  is  a  consequence 
of  the  deposit  of  micrococci.  They  are  all  little  bodies, 
not  more  than  the  one  twenty-five  thousandth  of  an  inch 
in  diameter.  They  are  very  minute,  therefore,  and  it  is 
claimed  that  this  deposition  in  the  endocardium  is  made 
up  in  very  considerable  degree  of  these  little  microscopic 
bodies.  That  would  only  bring  it  into  closer  affinity  with 
diphtheria  if  it  prove  to  be  true.  But  even  if  it  is  true 
I  do  not  believe  that  the  micrococci  are  micrococci  at  all. 
I  think  that  they  are  a  particular  form  of  deposit  of 
lymph  in  granular  shape,  and  certainly  there  is  no  proof 
that  they  are  vegetations.  It  is  a  mere  statement  of 
opinion  by  somebody,  and  that  opinion  has,  like  a  wave, 
spread  pretty  far.  I  am  willing  to  admit  that  the  subject 
is  under  judgment,  is  under  arbitration,  and  it  may  prove 
that  these  bodies  are  little  vegetations.  It  is  said  one 
divides  and  makes  of  itself  two,  and  the  two  divide  and 
make  of  themselves  four,  and  the  four  divide  and  make 
of  themselves  eight,  and  as  this  division  goes  on  pretty 
rapidly,  you  will  soon  get  high  numbers.  I  do  not  deny 
the  possibility  of  this  being  a  vegetation,  but  the  prob- 
ability of  its  being  a  vegetation  is  very  doubtful  in  my 
mind.  Stil\  ^hat  sort  of  thing  does  occur  in  the  endo- 
cardium ;  a  something  that  has  a  granular  form  is  deposited, 
and  afterward  leads  to  ulceration. 


Il6  MYOCARDITIS. 


LECTURE  IV. 

MYOCARDITIS. 

Now,  a  few  words  about  myocarditis ;  and  the  first 
word  I  have  to  say  is,  that  it  is  tautology.  We  duplicate 
upon  muscle.  Still,  it  is  a  term  that  has  become  current, 
and  we  must  meet  it  as  it  stands.  The  term  means  an 
inflammation  of  the  muscular  structure  of  the  heart,  and 
I  am  a  good  deal  in  doubt  whether  it  is  really  an  inflam- 
mation. 

There  you  observe,  in  this  upper  figure,  a  very  marked 
change  in  the  walls  of  the  left  ventricle.  Myocarditis 
produces  at  first  a  little  reddening  where  it  is  located,  and 
afterwards  it  comes  down  to  about  this  color.  The  disease 
is  local ;  it  does  not  affect  the  whole  heart  at  the  same 
time.  It  may  be  a  spot  that  you  can  cover  with  the  end 
of  your  finger — at  any  rate  with  the  palm  of  your  hand 
— rarely  larger.  Here  is  a  heroic  sort  of  thing.  I  ought 
to  have  shown  it  to  you  before.  It  is  a  heart  ruptured 
where  once  fatty  degeneration  occurred.  Upon  the 
exterior  here  is  a  spot  of  myocarditis  which  has  passed 
its  active  stage,  and  a  material  that  I  shall  describe  to 
you  pretty  soon  has  been  discharged  from  the  peri- 
cardium. If  you  lift  this  up  you  will  see  there  is  a  hole 
through  the  wall,  and  this  is  in  the  right  side — the  effects 
of  myocarditis,  but  not  myocarditis  itself. 

The  reason  why  I  doubt  whether  the  change  that  I  am 
going  to  describe  to  you  is  the  result  of  inflammation  is 
that,  so  far  as  is  known,  there  are  no  general  inflammatory 
symptoms  ;  no  particular  increase  in  the  frequency  of  the 
pulse ;  no  known  elevation  of  the  temperature  of  the  body. 


MYOCARDITIS.  11/ 

It  comes  on  quietly,  while  the  patient  is  attending  to  his 
business,  and  nothing  is  known  of  it  really,  except  by 
conjecture.  It  is  occasionally  found  to  follow  pericar- 
ditis and  endocarditis.  It  affects,  perhaps,  one  half  the 
thickness  of  the  muscular  structure  of  the  heart,  and  may 
occur  in  the  septum  ventriculorum,  or  it  may  occur  upon 
the  exterior  face  of  the  heart,  either  upon  the  left  or 
upon  the  right  side.  As  it  makes  its  progress  the  mate- 
rial that  is  effused  is  not  pus.  Examined  under  the  micro- 
scope it  seems  to  be  made  up  of  a  transparent  fluid  and 
broken-down  portions  of  the  heart  tissue.  It  seems  to  be 
rather  a  breaking  up  of  the  muscles  of  the  heart,  and  we 
can  conceive  that  it  may  be  by  obstruction  to  the  circu- 
lation of  the  blood  to  such  particular  part.  When  the 
disease  is  matured  you  find  what  you  would  call  a  little 
abscess,  and  what  has  always  been  called  heretofore  a 
little  abscess ;  but  the  material,  as  I  stated  to  you,  that 
constitutes  this  apparent  pus  is  not  made  up  of  pus  cor- 
puscles, but  debris.  •  This  material  is  so  fine  you  can  only 
recognize  its  quality  by  the  microscope.  It  at  length  is 
discharged,  either  outwardly  into  the  pericardium,  or  in- 
wardly into  the  cavity  that  it  may  be  affecting.  If  the 
latter  accident  occur,  it  may  do  mischief  in  the  way  of 
producing  embolism  in  distant  parts  of  the  system.  More 
frequently  it  is  evacuated  exterior  to  the  heart  and  within 
the  pericardium.  And  in  this  latter  case  it  seems  to  under- 
go absorption  and  is  carried  away,  no  remains  of  it  being 
left.  But  after  this  evacuation  of  the  debris  of  the  mus- 
cular tissue,  and  to  a  certain  extent  of  this  connective 
tissue,  there  is  a  chance  for  cicatrization.  The  connective 
tissue  which  covers  the  muscular  fibres  is  of  itself  suffi- 
cient to  start  a  healing  process,  and  if  the  heart  is  not 
overstrained  there  may  be  a  cicatrix  formed  over  the  de- 
pression ;  a  cicatrix  of  fibrous  tissue,  which,  of  itself, 
gives  strength  to  the  weakened  part  of  the  heart.      It 


Il8  MYOCARDITIS. 

may  rupture  before  this  cicatrix  is  formed  upon  it.  When 
the  heart  has  been  in  that  way  affected,  and  the  cicatriza- 
tion has  taken  place,  you  may  examine  it  at  post-mortem, 
and  find  that  it  has  not  ruptured — the  cicatrix  has  been 
a  protection  against  that ;  but  you  find  a  depression  cov- 
ered by  a  whitish  connective  tissue,  which  is  sometimes 
of  very  considerable  strength.  This  is,  in  substance,  my- 
ocarditis. And  you  can  see  now  how  myocarditis,  in  the 
particular  specimen  I  gave  you  last,  may  produce  a  weak- 
ening of  the  muscular  structure,  so  that  it  can  be  rup- 
tured. That,  together  with  the  effects  of  the  debris,  this 
mixed  matter,  upon  the  circulation  constitutes  the  whole 
of  the  bad  history  of  myocarditis.  There  is  a  certain 
amount  of  inflammation  of  the  heart  itself  when  there  is 
endocarditis  and  pericarditis,  as  I  have  already  told  you. 
The  most  common  result  of  that,  however,  is  simply  an 
infiltration,  into  the  muscular  tissue,  of  some  serum ;  a 
sort  of  oedema  of  the  heart,  which  readily  goes  away  after 
the  inflammation  has  passed  off.  It  is  only  in  rare  in- 
stances that  this  myocarditis  occurs  in  the  same  relation  ; 
that  is,  in  connection  with  endocarditis  and  pericarditis. 

It  occasionally  happens  that  a  part  of  the  wall  of  the 
heart  will  yield  to  the  contraction,  or  rather  to  the  pres- 
sure of  the  blood  upon  it,  and  pouch  out.  You  have  a 
plate  illustrating  that  now  in  your  hands.  That  however, 
was  a  thinning  of  an  already  thinned  heart ;  a  particular 
part  was  more  thinned  than  the  rest,  and  yielded,  so  as 
to  allow  a  pouch  to  be  formed  of  the  blood  within  the 
cavity.  More  commonly  these  aneurisms — for  they  are  so 
called — occur  in  the  inferior  and  right  portion  of  the  left 
ventricle.  It  becomes  pouched  out  toward  the  median 
line  and  downward.  This  occurs  sometimes  to  a  very 
considerable  extent.  And  it  will  form  clots,  layers  of 
coagulated  blood,  as  they  will  form  in  an  aneurism  of  the 
popliteal  space,  or  in  the   aorta,  or  in  any  other  part  of 


•V--  - ' 


MYOCARDITIS.  ^      1 19 

the  body.  As  the  blood  coagulates  in  this  expanded 
portion,  it  makes  a  covering  which  gives  a  certain  degree 
of  strength  to  this  weakened  part  of  the  heart.  After 
this  has  continued  for  a  considerable  time,  a  something  of 
a  white  color,  thick  and  resisting,  of  the  character  of  a 
cicatrix,  forms  upon  it  on  the  inside.  But  this  is  not  a 
cicatrix,  because  there  has  been  no  ulcerative  process. 
But  here  was  a  weakened  portion  of  the  heart,  and  nature 
seems  to  know  how  to  fortify  it,  and  on  the  endocardium 
there  is  thrown  out  a  certain  amount  of  lymph,  which  be- 
comes organized,  and  forms  a  new  membrane  of  the  con- 
nective tissue  variety.  You  do  not  see  that  in  this  plate. 
You  see  only  the  layers  that  have  been  separated  for  the 
purpose  of  illustration  ;  layers  of  coagulated  blood  that 
have  been  imposed  and  superimposed  upon  this  weakened 
part  of  the  heart,  and  they  are  torn  off  in  such  a  way  as 
not  to  show  you  exactly  the  relation  to  the  heart  itself. 

We  do  not  know  about  this  form  of  disease  during  life. 
It  is  found  almost  always  after  death.  We  can  find  an 
enlarged  heart,  and  from  the  extension  of  the  enlarge- 
ment in  a  particular  direction,  we  can  infer  that  it  is  of 
the  left  ventricle,  but  we  can  hardly  go  beyond  that.  A 
distinct  recognition,  before  death,  of  aneurism  of  the  heart 
as  it  usually  presents  itself  is  exceedingly  rare.  I  had 
lately — within  a  year,  I  think — a  very  remarkable  case  of 
aneurism  of  the  heart,  expanding  in  an  anterior  direction, 
and  pushing  its  way  through  the  intercostal  spaces  between 
the  fourth  and  fifth  ribs.  I  am  not  quite  sure  that  is  the 
point.  There  was  a  very  decided  pulsation.  It  was  a 
case  in  Dr.  Cole's  practice,  and  he  called  me  in  to  see  it, 
and  I  could  not  make  anything  out  of  it  but  aneurism  of 
the  heart.  It  could  not  have  been  aneurism  of  the  aorta, 
because  it  was  below  the  point  that  that  aneurism  occu- 
pies. It  pushed  the  ribs  forward  a  little,  and  formed  a 
cone  in  the  intercostal  space,  like  that  upon  the  heart  al- 


120  MYOCARDITIS. 

ready  shown  you.  Dr.  Cole  watched  this  patient  for 
some  months,  and  he  at  length  died  suddenly,  as  persons 
with  aneurism  are  apt  to  die ;  and  Dr.  Cole  asked  for  a 
post-mortem.  He  could  not  get  it.  The  friends  would 
not  consent  to  it.  He  went  to  the  coroner,  and  the  cor- 
oner came  and  inspected  the  body,  and  he  said,  "  Oh, 
yes,  this  is  aneurism.  We  know  aneurism  well  enough. 
A  post-mortem  is  not  necessary."  And  then  Dr.  Cole 
resorted  to  the  priest,  and  tried  to  induce  the  priest  to 
persuade  them  to  let  such  a  curious  thing  be  seen,  but 
the  priest,  even,  hadn't  the  power  to  persuade  them,  and 
the  mystery  was  buried  in  the  grave.  Still,  I  can  hardly 
entertain  any  doubt  that  it  was  of  this  kind.  Cases  of 
the  kind,  you  may  understand,  are  rare ;  still  in  the  enu- 
meration of  diseases  of  the  heart  ij:  seems  important  to 
say  a  few  words,  even  of  the  occurrence  of  a  rare  one. 

Dr.  Carl  Huber*  gives  a  number  of  cases  of  chronic 
myocarditis  and  disease  of  the  coronary  arteries,  in  which 
death  occured  suddenly,  or  with  only  preceding  constric- 
tion or  pain  in  the  chest ;  and  in  which  the  cause  of  death 
appeared  to  be  sclerosis  of  the  coronary  arteries  and  sub- 
sequent chronic  myocarditis.  The  consequences  of  this 
myocarditis  he  thinks  are  aneurism  of  the  heart,  throm- 
bosis, dilatation  and  hypertrophy.  The  symptoms  are 
angina  pectoris,  stenocardia,  and  asthma,  occurring  in 
paroxysms  usually  after  excitement,  physical  or  mental, 
sometimes  after  dinner.  In  some  there  is  irregularity  or 
intermittance  of  the  pulse,  sometimes  a  sudden  giddiness 
with  temporary  loss  of  consciousness  on  stooping,  walk- 
ing quickly,  or  going  upstairs ;  sometimes  there  is  col- 
lapse. It  has  nothing  to  do  Avith  endocardial  or  pericar- 
dial disease,  but  on  arterial  sclerosis.  The  general  cause 
is  alcoholism  or  syphilis. 

*  Med.  Re(.  July  28,  1885. 


MYOCARDITIS.  121 

Dr.  Beverly  Robinson  ^  read  a  paper  before  the  Practi- 
tioners* Society,  March  2d,  1883,  in  which  he  detailed  some 
cases  in  which  the  death  was  sudden  or  came  rapidly  in 
the  course  of  typhoid  fever  and  diphtheria,  and  one  or  two 
in  which  recovery  took  place  when  symptoms  had  ap- 
peared, which  in  other  similar  cases  had  ended  in  death. 
This  occurred  twice  in  one  patient,  and  in  others  once  or 
twice  before  the  fatal  sinking.  In  all  these  it  is  stated 
that  nothing  abnormal  could  be  discovered  by  examina- 
tion of  the  heart.  He  thinks  there  is  often  under  these 
circumstances  a  sudden  and  considerable  dilatation  of 
the  cardiac  cavities,  and  especially  of  the  right  heart,  and 
he  says,  "  Coagula  may  then  form,  or  if  the  heart  be  im- 
mediately and  strongly  stimulated,  the  imminent  stage 
may  be  tided  over." 

Dr.  Kinnicutt  said  that  in  various  acute  infectious  dis- 
eases, in  diseases  accompanied  by  high  temperature,  as 
well  as  in  pericarditis  and  endocarditis,  pathological  re- 
search had  demonstrated  the  very  frequent  existence  of  a 
parenchymatous  myocarditis.  The  inflammation  may  be 
diffused  or  circumscribed.  The  cardiac  muscle  became 
swollen  and  pale,  numerous  minute  granules  partly  solu* 
ble  in  acetic  acid  made  their  appearance  in  the  muscular 
fibre,  the  transverse  striae  become  indistinct,  and  finally 
disappear.  This  process  may  proceed  to  a  condition  of 
true  fatty  degeneration.  Might  not  these  changes  account 
for  some  of  these  sudden  heart  failures? 

Dr.  C.  S.  Dana  said  that  French  observers  had  recog- 
nized the  fact  that  in  acute  infectious  diseases  the  poison 
sometimes  especially  attacks  the  heart.  In  typhoid  fever 
a  "  cardiac  form"  has  been  described.  Sudden  deaths 
pccur  also  in  nephritis  and  pneumonia. 

>'-J      'r  ,, — ■ — r- — 

f  JliQ  Medicql  Record,  IVlay  §,  ;88^. 


122  HYPERTROPHY  OF  THE  HEART. 


LECTURE  V. 

HYPERTROPHY   OF  THE   HEART. 

When  I  was  a  student  of  medicine  hypertrophy  was 
described  under  three  divisions :  First,  simple  hypertro- 
phy ;  second,  eccentric  hypertrophy  ;  and  third,  concen- 
tric hypertrophy.  We  do  not  use  those  terms  now.  It 
is  hypertrophy,  and  hypertrophy  with  dilatation.  Hy- 
pertrophy with  contraction,  concentric  hypertrophy,  is 
probably,  in  every  instance,  no  hypertrophy  at  all.  The 
last  act  of  the  heart  was  to  contract,  and  to  force  out  the 
blood  that  was,  just  the  instant  before,  within  its  cavity. 
It  is  very  much  contracted,  its  cavity  is  nearly  obliterated 
and  it  may  be  taken  for  a  diseased  condition.  But  it  is 
a  natural  office  of  the  heart  to  contract,  and  if  death 
strikes  at  the  instant  that  the  contraction  is  completed  you 
will,  of  course,  find  no  blood  in  the  ventricles  of  the  heart : 
you  will  find  it  smaller  than  natural,  and  that  would  not 
be  consistent  with  the  term  hypertrophy.  The  walls  are 
thicker  because  they  are  contracted.  I  think  it  would  be 
found  that  every  instance  that  was,  of  old,  called  concen- 
tric hypertrophy  could  be  resolved  into  the  condition 
that  I  have  described.  So  that  now  we  have  hypertrophy, 
and  hypertrophy  with  dilatation. 

The  first  question  that  presents  itself  is,  what  is  hyper- 
trophy of  the  heart  ?  Well,  the  obvious  answer  is,  enlarge- 
ment of  its  walls  ;  increase  in  the  bulk  of  matter  that 
constitutes  the  walls  of  the  heart.  Well,  what  constitutes 
the  walls  of  the  heart?  Mainly,  muscular  fibres,  and 
some  connective  tissue.  Then  it  is  the  muscular  fibres  of 
the   heart   that   are   increased ;   and  how  increased  ?     I 


HYPERTROPHY  OF  THE   HEART.  1 23 

asked  myself  that  question  a  great  many  years  ago,  and  I 
resorted  to  some  old  specimens  I  found  at  the  hospital 
for  the  answer.  A  point  to  be  investigated  was,  the  size 
of  the  muscular  fibre  in  hypertrophy  of  the  heart ;  is  it 
larger  than  the  muscular  fibre  in  the  heart  of  natural  size? 
I  procured  about  twenty  or  twenty-five,  and  drew  fibres 
from  different  parts  of  the  heart,  from  one  ventricle,  and 
then  from  the  other,  and,  compared  those  from  the  nat- 
ural heart  with  those  from  the  hypertrophied  heart,  and 
though  occasionally  I  would  find  enlarged  fibre  the  average 
was  pretty  nearly  the  same  in  the  healthy  and  in  the  hy- 
pertrophied heart.  Well,  then,  the  conclusion  is  inevita- 
ble that  if  the  same  proportion  exists  between  the  size 
of  the  muscular  fibre  of  the  natural  and  of  the  hypertro- 
phied heart,  there  must  be  a  multiplication  of  the  fibres 
of  the  muscles  in  the  latter,  and  that  is  a  fact.  There 
is  a  new  production  of  muscular  fibres.  From  what 
origin  they  spring  I  cannot  tell  you,  but  nature  has  so  ar- 
ranged it  that  if  the  heart  needs  additional  strength  it 
can  get  additional  fibres. 

The  size  to  which  the  heart  may  grow  is,  perhaps, 
limited  to  sixty  ounces.  When  we  meet  next  I  intend  to 
show  you  one  that  weighed  fifty-seven  ounces — within 
three  ounces  of  the  largest  heart  the  weight  of  which  has 
been  recorded.  The  natural  weight  of  a  heart  in  a  full 
grown  person,  not  remarkably  broad  upon  the  shoulders, 
is  eleven  ounces ;  if,  then,  it  is  increased  to  sixteen  or 
eighteen  ounces,  you  see  there  is  some  hypertrophy ;  if  it 
is  increased  to  twenty-five  or  thirty,  there  is  very  consid- 
erable hypertrophy ;  and  if  it  is  increased  to  anywhere  in 
the  neighborhood  of  sixty  ounces  it  is  cors  bovinmn,  an  ox- 
heart,  and  here  I  may  say  that  that  enormous  size  is 
never  attained  except  in  persons  in  whom  disease  of  the 
heart  began  in  infancy.  This,  the  largest  heart  I  possess, 
perhaps  the  largest  heart  in  the  country,  was  taken  from 


124  HYPERTROPHY   OF  THE   HEART. 

a  man  who,  at  six  years  of  age,  was  taken  over  by  his 
physician  from  Randolph,  Vermont,  to  Dr.  Nathan 
Smith,  and  was  shown  by  him  as  an  instance  of  heart  dis- 
ease arising  from  inflammatory  fever,  rheumatism.  The 
boy  had  had  articular  rheumatism,  and  his  heart  became 
involved,  and  Dr.  Nathan  Smith  had  interest  in  it  as 
an  instance  showing  there  might  be  some  connection  be- 
tween articular  rheumatism  and  disease  of  the  heart.  It 
was  fourteen  years  after  that — more  than  that — -twenty 
odd  years,  before  the  connection  between  articular  rheu- 
matism, pericariditis,  and  endocarditis  was  made  out ;  so 
that,  really,  had  it  been  published,  that  discovery  of  Dr. 
Smith  would  have  been  put  first,  as  showing  the  relation 
between  rheumatism  and  inflammatory  affections  of  the 
heart.  The  boy  grew  up,  attained  the  age  of  twenty- 
eight  years,  and  to  show  you  his  was  not  a  useless  heart, 
he  was  foreman  of  a  manufactory  in  the  immediate  neigh- 
hood  of  Springfield,  Mass.  He  was  only  incapacitated 
for  work  about  a  month.  He  kept  his  men  all  in  line,  all 
at  work,  until  his  breath  became  so  short,  probably 
through  involvement  of  the  kidneys,  that  it  was  so  painful 
to  him  he  was  forced  to  give  it  up.  He  remained  at 
home  after  that,  and  died  about  a  month  after  ceasing  to 
work,  and  yet  carried  this  enormous  Heart.  I  have  never 
seen  a  very  large  heart  in  a  person  in  whom  it  did  not 
begin  to  grow  in  early  life. 

The  heart  may  be  hypertrophied  in  the  wall  of  one  of 
its  cavities.  The  hypertrophy  usually  found  about  the 
heart  is  that  of  the  walls  of  the  left  ventricle.  The  left 
ventricle  is  hypertrophied  oftener  than  any  other  portion 
of  the  heart.  You  will  find,  also,  hearts  that  are  hyper- 
trophied in  all  of  the  cavities ;  perhaps  some  such  among 
those  that  I  shall  show  you  at  our  next  meeting ;  and 
others,  perhaps,  that  are  hypertrophied  in  the  two  ventri- 
cles ;  and  one  or  two,  I  think  I  have,  that  are  hypertro- 


HYPERTROPHY   OF  THE   HEART.  12$ 

phied  in  the  right  ventricle,  the  right  auricle,  and  the  left 
ventricle.  So  that  hypertrophy  may  be  single,  or  it  may 
occupy  each  one  of  the  walls  of  the  heart  cavities. 

The  causes  of  hypertrophy  are  various.  The  most 
common  cause  is  the  need  of  more  strength  in  the  walls 
of  the  cavity  that  is  immediately  affected.  Obstruction,, 
then,  at  the  aortic  opening,  as  has  already  been  stated  ta 
you,  is  attended  by  hypeftrophy;  but  the  heart  does  not 
seem  to  know  exactly  when  to  stop  growing,  though  it 
does  know  when  to  begin  to  grow,  and  it  may  go  on  to 
become  diseased.  A  moderate  hypertrophy,  then,  with 
obstruction  at  the  aortic  opening,  may  not  be  regarded 
as  a  grave  disease.  Then,  regurgitations  will  lead  to 
hypertrophy.  That  the  obstruction  not  requiring  in- 
creased strength  in  the  walls  of  a  cavity  will  not  produce 
hypertrophy,  you  will  see  in  the  fact  that  stenosis  of  the 
mitral  valve  is  attended  by  no  change  in  the  left  ventricle. 
If  there  is  regurgitation,  then  the  left  ventricle  may 
become  hypertrophied.  It  needs  more  strength  for  the 
work  it  has  to  do.  But  if  it  is  simply  an  obstruction  of  the 
blood  coming  from  the  left  auricle  into  the  left  ventricle, 
and  the  left  ventricle  becomes  in  the  end  fairly  filled,  and 
does  not  throw  the  blood  back  again  into  the  auricle,  then 
there  is  never  any  hypertrophy  of  the  left  ventricle.  It  is 
only  in  regurgitation  with  this  lesion  that  hypertrophy 
comes.     Here,  then,  is  one  cause. 

Another  cause  is  increased  strain  upon  the  heart ;  an 
increased  demand  continued  for  a  long  time,  attended  by 
a  nutritive,  non-deteriorated  condition  of  the  blood.  You 
see  why  I  make  that  limitation ;  because  a  man  with 
typhoid  fever  may  have  his  heart  beating  rapidly  and 
pretty  strongly  for  four  weeks  continuously,  and  no 
hypertrophy  follow.  But  then  his  blood  is  deteriorated  ; 
all  his  tissues  are,  throughout.  If  by  mental  or  physical 
excitement  his  heart  should  beat  this  way,  at  the  same 


126  HYPERTROPHY   OF  tPIE   HEART. 

rate  and  for  the  same  length  of  time,  and  his  blood  were 
in  a  nourished  condition,  his  heart  would  become  hyper- 
trophied  to  a  certain  extent.  Disease  that  produces 
increased  action  of  the  heart  and  full  action  of  the  heart, 
does  not,  then,  cause  hypertrophy,  unless  the  blood  is  in 
good,  full,  nutritive  condition.  Occupations  that  are  at- 
tended by  great  mental  excitement  and  by  heart  beating 
are  dangerous  in  this  respect,  producing  hypertrophy 
without  valvular  disease.  The  little  tyrants  that  command 
on  vessels  at  sea  sometimes  are  very  passionate  men.  I 
have  seen  them  beat  their  men  about  and  swear  at  them 
as  if  they  belonged  to  orur  army  of  Flanders ;  and  those 
men  are  very  apt  to  get  hypertrophy  of  the  heart.  They  do 
not  observe  the  rule  of  Scripture,  let  not  the  sun  go  down 
upon  thy  wrath.  They  are  wrathful  at  night.  A  French 
physiologist  has  interested  himself  in  the  cardiac  condi- 
tion of  the  domestic  fowl,  and  he  found  that  where  one 
rooster  had  to  be  the  husband  of  ten  or  twelve  hens,  he 
was  apt  to  get  hypertrophy  of  the  heart.  This  may  be  a 
warning  in  regard  to  sexual  indulgence. 

Then,  again,  hypertrophy  comes  from  causes  that  are 
not  known.  We  say  in  general  that  it  is  an  error  of  nu- 
trition, but  why,  we  do  not  know.  Persons  of  quiet  tem- 
per and  of  easy  life,  not  subject  to  particular  excitements, 
and  having  no  valvular  disease  of  the  heart,  do  once  in  a 
while  get  hypertrophy  of  the  heart ;  but  it  is  uncommon  ; 
decidedly  uncommon. 

The  time  seems  to  be  passed  when  it  was  necessary  to 
ascertain  the  effect  of  the  contracted  kidney  on  the  heart 
by  experiment  on  animals.  There  appears  to  be  very 
general  assent  to  the  proposition  that  it  causes  hyper- 
trophy of  the  left  ventricle.  But  in  the  reports  of  those 
who  have  studied  the  matter  experimentally  there  is  a 
remarkable  disagreement,  and  it  is  worthy  of  notice  that 


HYPERTROPHY   OF   THE    HEART.  12/ 

while  the  clinical  studies  have  been  settling  the  question 
the  experimental  should  be  so  inharmonious. 

Dr.  Straus,  of  Paris,  tied  one  ureter  in  twenty  guinea 
pigs  to  cause  atrophy  of  the  kidney  to  which  it  belonged. 
These  animals  were  killed  four  to  six  months  after  this 
was  done,  and  the  left  ventricle  was  found  enlarged  in 
every  one  of  them.  The  hypertrophy  was  not  great — 
only -J-  to  J  the  original  weight,  but  the  time  was  short. 
The  muscular  fibres  were  healthy. 

Grawitz  and  Israel  asserted  that  while  hypertrophy  of 
the  heart  might  follow  a  kidney  lesion  in  old  animals  in 
which  the  other  kidney  did  not  grow  to  compensation 
this  result  was  not  to  be  obtained  in  young  animals.  But 
nearly  all  of  Dr.  Straus'  animals  were  young. 

Rollet  *  records  the  following  case  of  hypertrophy  con- 
fined to  the  left  ventricle,  the  walls  of  which  were  pale  and 
presented  here  and  there  small  spots  of  sclerosed  tissue. 
The  aortic  orifice  was  normal.  A  fibrous  band  was  found 
extending  from  the  under  surface  of  the  aortic  lip  of  the 
mitral  valve  to  the  intraventricular  septum  and  aortic 
portion  of  the  ventricle  at  a  little  distance  from  the  sig- 
moid valves.  The  new  growth  narrowed  the  aortic  cone  to 
such  an  extent  that  one  finger  could  with  difficulty  be  in- 
troduced. The  author  thinks  this  band  was  produced  by 
endocarditis  before  birth.  A  similar  case  affecting  the 
right  ventricle  is  recorded  by  Dettrich,  1849. 

The  patient  was  a  woman  forty-seven  years  of  age,  ad- 
mitted with  palpitations,  thoracic  pain,  dyspnoea  and 
cephalalgia ;  cardiac  rhythm  irregular.  There  was  an  in- 
creased area  of  dulness,  apex  beat  strong  and  to  the  left 
of  its  normal  place.  There  was  a  distinct  thrill,  percepti- 
ble only  under  the  lower  part  of  the  sternum,  to  the  left 
of  that  bone  and  at  the  apex.     There  was   a  rather  pro- 

*  The  Medical  Record,  Oct.  7,  1882. 


l^B  HYPERTROPHY  OF  THE  HEART. 

longed  systolic  murmur  of  greatest  intensity  in  the  fourth 
interspace  at  the  left  border  of  the  sternum.  The  second 
sound  was  audible  at  the  base  and  in  the  carotid,  showing 
the  integrity  of  the  sigmoid  valves. 

Now  the  question  comes,  how  to  recognize  hypertrophy 
of  the  heart.  A  heart  like  that  one  that  is  passing  around, 
which  I  told  you  is  hypertrophied,  occupied  a  greater 
space  in  the  chest  than  it  did  when  it  was  of  normal  size, 
and  what  will  that  do  ?  It  will  crowd  the  lung  away.  The 
space  over  which  a  heart  of  natural  size  will  practically 
come  in  contact  with  the  walls  of  the  chest,  or,  in  other 
words,  not  be  covered  by  lung,  is  about  equal  to  two  su- 
perficial inches ;  but  when  a  heart  grows,  as  that  has,  it 
must  crowd  the  lung  out  of  position.  In  a  healthy  per- 
son you  can  hear  the  respiratory  murmur  over  the  whole 
praecordial  region  ;  but  when  you  listen  to  a  person  who 
has  considerable  hypertrophy  of  the  heart  you  will  very 
likely  fail  to  find  the  respiratory  murmur  over  the  anterior 
portion  of  the  heart,  because  the  lung  has  been  crowded 
away.  That  comes  to  be,  then,  one  sign  for  the  recogni- 
tion of  it.  The  same  thing,  however,  occurs  when  the 
pericardium  is  dilated  with  fluid.  The  lung  then  is  neces- 
sarily crowded  away  in  the  same  manner. 

Another  point  is  that  the  region  of  dulness  is  in- 
creased more  or  less  markedly.  The  point  to  which  the 
apex  of  the  heart  can  be  pushed  to  the  left  by  its  hyper- 
trophy is  perhaps  six  inches  and  a  half  from  the  median 
line.  Then  you  get  to  about  the  outer  curve,  the  outer 
limit  of  the  curve  of  the  chest.  It  may  be  pressed  back- 
ward beyond  that,  but  I  do  not  remember  to  have  meas- 
ured a  heart  which  extended  to  the  left  more  than  six 
inches  and  a  half.  I  have  found  it  six  inches  a  great 
many  times,  and  five  inches  and  a  half  a  great  many 
times.  You  can  measure  it  in  either  one  of  two  ways. 
Find  the  apex,  and  be  sure  that  there  is   no  heart  beat 


HYPERTROPHY   OF  THE   HEART.  I 29 

beyond  that,  and  you  can  pretty  safely  measure  up  to 
that  point  from  the  median  line.  But  it  is  always  better 
to  make  percussion,  so  that  you  will  be  sure  of  the  point 
to  which  you  should  measure.  Dulness  over  the  lung 
upon  an  enlarged  lieart  is  very  decided.  The  line  of 
division  between  them  is  pretty  clearly  cut.  Yet,  even 
suppose  you  get  dulness  over  six  inches  from  the  median 
line,  your  diagnosis  is  not  yet  made.  The  same  thing  may 
happen  with  pericarditis  and  an  enlarged  pericardium. 
Then  seek  for  the  apex  of  the  heart.  If  there  is  marked 
enlargement  of  the  right  side  of  the  heart  the  apex  will 
be  tilted  up  toward  the  axilla.  It  will  be,  perhaps,  as 
high  as  the  fifth  rib,  following  the  curve  of  the  rib  up- 
ward, or  it  may  not  be  as  high  as  that.  Its  direction  is 
upward  and  outward,  and  to  the  left.  If  it  is  the  left 
side  of  the  heart  exclusively  that  is  hypertrophied,  the 
apex  may  be  situated  in  the  seventh  intercostal  space, 
outward,  downward,  and  to  the  left.  Of  course  it  will 
be  in  the  sixth  before  it  is  in  the  seventh.  It  is  in  the 
intercostal  space,  of  course,  that  you  can  most  easily  feel 
the  impulse  of  the  heart.  And  then,  again,  you  must 
make  percussion  to  verify  the  indications  of  the  apex- 
beat.  There  is  nothing  that  is  likely  to  trouble  you  in 
the  attempt  at  diagnosis  but  pericarditis.  It  is  true,  the 
heart  is  sometimes  the  seat  of  tumors ;  and  the  pericar- 
dium becomes  enlarged  sometimes  by  air,  but  that  will 
not  give  dulness.  In  general  practice,  with  the  exception 
of  the  extraordinary  cases,  that  you  do  not  expect  to 
see,  these  two  things  will  give  you  the  only  trouble  there 
will  be.  Hypertrophy  is  otherwise  easily  recognized. 
There  is  a  point,  however,  to  be  borne  in  mind.  I  examined 
a  gentleman  yesterday  who  had  been  educated  to  the 
profession,  but  had  gone  into  business.  He  had  pleurisy 
filling  the  left  side  of  the  chest,  and  his  heart  was  pushed 
over  so  that  the  apex  beat  was  about  in  the  position  on 


I30  HYPERTROPHY   OF   THE   HEART. 

the  right  side  that  it  would  naturally  occupy  on  the  left, 
crowded  over  by  this  accumulation  of  fluid  in  the  left 
side  of  the  chest.  Now,  a  person  who  has  hypertrophy 
of  the  heart  may  have  pleurisy  as  well  as  anybody  else, 
and  the  heart  may  be  displaced  in  the  same  way.  It 
may  be  displaced  to  the  left  also.  An  effusion  upon  the 
right  side  will  encroach  upon  the  right  side,  will  encroach 
upon  the  mediastinum  sufficiently  to  crowd  the  heart 
over  an  inch  further  to  the  left  than  it  naturally  would  be. 
Such  a  case  as  that  you  may  mistake  for  hypertrophy 
when  it  is  only  a  displacement.  It  will  be  important  to 
know,  then,  whether  there  is  any  effusion  upon  the  right 
side  of  the  chest. 

Then,  again,  the  history  of  hypertrophy  and  of  peri- 
carditis will  be  found  different.  Hypertrophy  is  a  chronic 
affection,  and  a  man  who  has  it,  and  is  sent  to  you  for  it, 
will  have  had  for  a  good  while  some  shortness  of  breath 
in  going  up  stairs.  Then,  again,  the  dulness  extends,  in 
pericarditis,  as  I  have  already  told  you,  in  a  direction  dif- 
ferent from  the  dulness  in  hypertrophy.  You  get  a  cer- 
tain degree  of  dulness  in  pericarditis,  with  copious  effu- 
sion, on  the  right  side  of  the  sternum,  and  you  get  it 
above  the  third  rib.  It  is  only  effusion  in  the  pericardium 
that  does  that.  The  physical  signs  of  hypertrophy,  there- 
fore, are  pretty  clearly  made,  pretty  clearly  cut,  and  you 
need  hardly  make  any  mistake  about  it. 

The  rational  signs  are  more  obscure.  You  cannot  be 
sure,  by  any  study  of  the  general  symptoms,  that  you 
have  hypertrophy  and  nothing  else.  You  can  pretty 
easily  determine,  from  the  rational  symptoms,  that  there 
is  heart  disease,  but  exactly  what  it  is,  is  almost  impossi- 
ble to  determine.  The  usual  symptoms  of  heart  disease 
are  to  be  observed  in  these  patients — that  is,  a  certain  de- 
gree of  shortness  of  the  breath  on  exertion,  frequently  a 
disposition  to  rest  the  head  on  two  or  three  pillows,  in- 


HYPERTROPHY   OF  THE   HEART.  I3I 

stead  of  one,  in  sleep  ;  a  disinclination  to  sleep  upon  the 
right  side  of  the  body,  not  because  it  gives  them  pain, 
but  because  it  disturbs  them,  it  makes  them  nervous; 
they  feel  the  heart  beat,  and  that  makes  them  nervous. 
Palpitation  cannot  be  relied  on  as  a  means  to  distinguish 
hypertrophy.  It  is  wonderful  how  much  of  thumping 
the  heart  will  have,  and  the  patient  be  entirely  unaware 
of  it  in  some  instance ;  afid  it  is  really  surprising  how  lit- 
tle of  real  palpitation  will  give  other  persons  much  un- 
easiness. There  is  a  real  palpitation  and  there  is  a  sub- 
jective palpitation.  Persons  of  particular  habits  will  be- 
come nervous  and  feel  palpitation  when  there  is  only 
natural  action  of  the  heart.  It  arises  alone  from  their  in- 
creased sensitiveness  or  the  heightened  state  of  nervous 
perception.  And  then,  as  I  said  before,  a  man  who  has 
real  hypertrophy  of  the  heart,  who  has  been  accustomed  to 
hard  knocks  in  life,  may  pay  no  attention  to  it,  while  it 
may  lift  your  head  half  an  inch  at  each  beat  when  you 
apply  your  head  to  the  chest.  It  knocks  like  a  hammer 
against  the  face  and  ear  ;  and  yet,  ask  him  if  his  heart 
palpitates.  "  O  no,  O  no,  my  heart  is  good  !"  But  pal- 
pitation is  not  a  certain  guide  to  diagnosis.  The  man 
we  saw  at  the  clinic  yesterday  had  no  palpitation  ;  that  is, 
nothing  that  you  could  feel  with  the  hand.  You  could 
feel  that  the  heart  was  beating,  but  not  with  extraordinary 
force.  He  had  had  his  disease  for  a  considerable  time, 
and  it  is  to  be  presumed  that  the  heart  had  lost  some  of 
its  energy.  But  even  in  persons  in  whom  the  disease 
may  be  gradually  growing  there  may  be  decided  palpi- 
tation, and  there  may  not  be,  so  that  you  will  have  to 
consider  what  is  the  cause  of  the  palpitation,  if  you  find 
it.  * 

Shortness  of  breath  is  common  to  almost  all  the  forms 
of  cardiac  disease,  so  that  there  is  nothing  particularly 
distinctive  in  that.     Then  comes  the  question,  what  can 


132  DILATATION   OF  THE   HEART. 

be  done  for  the  relief  of  these  patients  ?  and  then,  again, 
as  all  the  diseases,  or  nearly  all  the  diseases,  of  the  heart, 
have  about  the  same  physical  history,  their  treatment  will 
be  substantially  the  same,  so  that  I  will  say  what  is  to  be 
said  about  that  further  on. 


B 


LECTURE  VI. 

DILATATION  OF  THE   HEART. 

There  is  another  condition  of  the  heart  that  deserves 
particular  attention.  I  say  particular,  as  it  is  not  nearly 
so  common  as  hypertrophy  with  dilatation.  It  is  dilata- 
tion alone,  and  this  brings  me  to  the  question,  what  pro- 
duces dilatation  of  the  heart,  whether  it  occurs  with  hy- 
pertrophy or  singly  ?  The  answer  to  this  question,  I 
think,  has  been  given  by  Niemeyer:  dilatation  of  the 
heart  is  caused  by  a  reflux  of  blood  into  it,  which  blood 
has  just  been  thrown  out  of  a  cavity.  For  example,  the 
blood  is  thrown  into  the  aorta,  there  is  a  reflowing,  a  re- 
flux of  it  into  the  ventricle ;  perhaps  one  half  of  it  that 
was  thrown  out  comes  back  again,  and  this  is  in  the  pe- 
riod of  non-resistance  of  the  heart  ;  its  muscle  is  all  re- 
laxed, flabby.  If  it  were  to  come  during  contraction  there 
would  be  resistance  to  enlargement,  but  the  muscle  is,  so 
to  speak,  dead  at  the  moment ;  it  is  in  the  period  of  re- 
pose that  this  reflux  takes  place.  It  stretches  it,  together 
with  the  blood  flowing  in  from  the  auricle.  It  is  com- 
pelled to  contain  more  than  it  was  made  to  contain,  and 
the  result  is  a  moderate  dilatation,  and  this  continued 
seventy-two  times  a  minute,  for  days,  and  weeks,  and 
months,  will  produce  an  effect.  One  occurrence,  proba- 
bly, would  not  be  felt,  but  a  repetition  is  what  produces 


DILATATION   OF  THE   HEART.  1 33 

the  dilatation.  Well,  this  dilatation,  then,  is  caused  by 
an  unnatural  flow  of  blood  into  the  ventricle,  and  the 
heart,  feeling  its  contents,  naturally  acts  with  more  than 
ordinary  force,  so  that  hypertrophy  and  dilatation  often 
go  together,  step  by  step. 

Dr.  Peabody  *  showed  to  the  N.  Y.  Pathological  So- 
ciety a  heart  of  which  the  following  is  a  description  :  The 
endocardium  was  generally  thickened,  as  were  the  aortic 
cusps.  The  chief  lesion  was  in  the  muscle  of  the  heart. 
It  had  been  replaced  by  connective  tissue  largely  in  two 
places ;  the  most  marked  was  a  circular  spot  of  nearly  two 
inches  in  diameter  between  the  papillary  muscle  and  the 
attachment  of  the  aortic  valve,  and  there  was  distinct 
aneurismal  bulging  of  the  septum  ventriculorum  and  also 
of  the  left  border  of  the  left  ventricle.  The  depth  of  the 
sac  was  three  quarters  of  an  inch.  A  second  sac  was 
near  the  apex  of  the  ventricle  in  the  septum.  The  mus- 
cular tissue  was  in  the  state  of  brown  atrophy.  The 
coronary  arteries  open  at  their  origin ;  their  branches 
were  obstructed  or  occluded  by  a  growth  from  their 
lining  membrane.  Patient  was  a  man  fifty-five  years 
old. 

I  told  you,  in  speaking  of  hypertrophy,  that  I  would 
show  you  a  heart  that  is,  probably,  the  largest  that  has 
been  noticed  in  this  country.  This  is  the  specimen. 
There  are  several  interesting  things  about  this  :  first,  that 
it  is,  probably,  \h.e  largest  heart  that  has  been  in  this 
land  ;  second,  its  history  is  well  preserved.  I  gave  you 
the  history  in  a  previous  lecture.  The  patient  could  carry 
this  large  heart  only  because  he  grew  up  with  it.  These 
large  hearts,  as  far  as  I  have  noticed,  always  begin  to  be 
diseased  in  early  childhood,  possibly  in  infancy,  and  the 
person  becomes  accustomed  to  the  extraordinary  develop- 

*  Medical  Hecord,  July  29,  1882. 


134  DILATATION  OF   THE   HEART. 

ment,  and  so  it  gives  little  inconvenience.     It  grows  with 
his  growth,  and  may  attain  this  monstrous  size. 

I  told  you,  when  speaking  of  pericarditis,  that  I  would 
exhibit  to  you  a  heart  to  which  the  pericardium  was  at- 
tached.    You  observe  here  is  the  pericardium,  and  it  is 
attached  to  the  heart.     The  patient  had  had  endocarditis 
and  pericarditis,  and  this  is  an  instance  in  which  we  can 
pretty  safely  say  we  have  twenty-two  years  from  devel- 
opment of  the  pericarditis  till  death.     You  will  see  the 
manner  in  which  the  pericardium  is  trying  to  separate  it- 
self from  the  heart.     By  just  raising  up  the  flap  of  this 
pericardium  on  either  side  you  will  see  threads  running 
from  one  side  to  the  other.     They  have  been  considera- 
bly torn  up  by  handling,  but  still  I  think  you  will  notice 
them  better  on  the  upper  side.     This  pericardium,  had 
the  man  lived  long  enough,  would  have  been  separate. 
The  attachment,  as  you  see,  is  loose.     Then,  as  a  speci- 
men of  aortic  disease,  it  is  extraordinary.     Opening  the 
aorta  by  ''  its  ears,"  and  getting  down  to  the  valves,  you 
see  they  are  thick  and   leathery.     They  are  more  than  a 
Hne  in  thickness,  nearly  an  eighth  of  an  inch  in  thickness, 
and  they  are  much  distorted,  and  are,  you  see,  quite  inca- 
pable of  performing  their  office.     They  feel  hard,  like  sole 
leather.     Then  the  right  auricle,  together  with  the  right 
ventricle,  you   observe,   is  somewhat    dilated,  but    very 
much  encroached   upon  by  the   septum  ventriculorum. 
The  mitral  valve  is  not  so  very  much  diseased.     That  is 
to  say,  its  offices  are  not  very  much  hindered.     It  is  thick, 
scarcely  leathery,  its  posterior  valve  is  contracted.     It  is 
contracted  considerably,  and  I  am  not  sure  that  it  would 
perform  its  office  perfectly.     But  the  amount  of  disease 
there  is  trifling  compared  with  that  which  effects  the 
aortic  valves. 

Here,  too,  has  been  pericarditis.     You  observe  how 
rough  the  heart  is.     There  is  something  of  that  thready 


DILATATION   OF  THE   HEART.  1 35 

appearance,  not  so  much,  however,  as  in  the  other  speci- 
men, in  this  pericardium.  I  do  not  know  the  history  of 
this  case  as  I  do  that,  but  you  observe  here  is  very 
marked  shortening  of  the  valve.  That  valve  is  not  one 
half  its  proper  height,  and  it  would  be  impossible  for  its 
parts  to  meet  in  the  middle  of  the  artery  and  prevent  re- 
gurgitation. In  this  instance  the  right  heart  is  more  hy- 
pertrophied  than  the  left — that  is,  in  proportion  to  its 
natural  thickness  the  walls  are  thicker,  and  in  regard  to 
capacity  it  seems  to  be  just  about  as  great  as  the  left. 
The  thickening  here  is  quite  remarkable.  The  tricuspid 
valve  does  not  seem  to  be  diseased.  The  aortic  valve  is 
firm,  and  shortened  to  a  certain  extent,  and  here  again 
the  posterior  more  than  the  anterior  curtain  of  the  valve. 
But  the  great  defects,  or  rather  the  principal  diseases  of 
the  heart,  are  the  hypertrophy,  particularly  of  the  right 
side,  and  the  valvular  disease  at  the  aortic  opening.  The 
pulmonary  valves  are  about  natural. 

Here  is  another  specimen  of  marked  hypertrophy,  and 
here  again  you  observe  a  septum  of  the  aortic  valve 
thickened  and  drawn  down.  The  valves,  you  observe, 
are  very  imperfect,  and  allowed  regurgitation,  while  the 
mitral  valve  is  in  tolerably  good  condition.  The  right 
ventricle  is  small,  comparatively.  It  will  not  hold  one 
half,  it  will  hardly  hold  a  quarter  of  what  the  left  will, 
and  that  of  itself  is  a  kind  of  disease.  The  blood  can  be 
thrown  out  from  the  left  heart  a  great  deal  more  rapidly 
than  it  can  be  received  by  the  right ;  and  the  result  is 
exactly  the  same  as  when  the  valves  are  defective. 

I  was  speaking  to  you,  w^hen  we  were  last  together,  of 
dilatation,  I  had  begun  to  describe  to  you  the  peculiari- 
ties of  that  disorder  of  the  heart.  We  will  go  on  with 
that,  and  I  will  show  you  at  our  next  meeting  a  speci- 
men that  is  rather  striking ;  a  dilated  heart,  in  which,  if  I 
remember  right,  all  the  cavities  are  dilated,  and  they  are 


136  DILATATION  OF  THE  HEART. 

stuffed  with  hair,  so  that  the  heart  has  about  the  size 
that  it  had  in  life,  and  yet  in  the  cuts  made  into  the  walls 
you  will  see  to  what  a  very  marked  thinness  it  has  been 
reduced. 

Dilatation,  I  told  you,  considering  it  in  the  sense  in 
which  we  are  using  the  word  now,  is  a  thinning  of  the 
walls  of  the  heart.  We  have  hypertrophy  with  dilatation, 
in  which  there  may  be  considerable  thickening  of  the  walls 
of  the  heart,  but  this  is  spoken  of  by  a  distinctive  name. 
We  now  refer  to  simple  dilatation  of  the  heart,  in  which 
the  walls  of  the  heart  of  the  left  side  come  to  be  little 
more  than  a  line  in  thickness.  The  walls  of  the  right 
heart  are  from  three  to  five  lines  in  thickness  in  the  nor- 
mal state,  that  is,  three  at  about  half  an  inch  from  the 
base,  and  growing  a  little  thicker  toward  the  apex,  and 
at  the  apex  five  lines  in  thickness.  But  this  heart  that 
I  shall  exhibit  to  you  at  our  next  meeting  will  give  less 
than  a  line  in  thickness  of  any  portion  of  the  left  ventricu- 
lar wall. 

The  first  question  that  presents  itself  to  us  is,  how  can 
this  thinning  occur?  A  good  many  speculations  have 
been  offered  in  explanation  of  this  occurrence,  but  I  am 
inclined  to  think  that  the  German  explanation  is  the 
best :  that  it  may  occur  in  two  different  ways :  First,  by 
a  reflux  of  blood  when  the  blood  is  in  a  non-nutritive 
state,  dilating  the  natural  walls  of  the  heart  till  they  are 
thinned  down  to  a  condition  I  shall  exhibit  to  you  ;  the 
other,  that  hypertrophy  with  dilatation  may  have  oc- 
curred, and  that  by  fatty  degeneration,  which  I  shall  ex- 
plain to  you  a  little  further  on,  the  material  constituting 
the  muscle  of  the  heart  may  be  absorbed,  taken  up,  car- 
ried away,  leaving  very  little  but  the  two  serous  mem- 
branes, the  endocardium,  and  the  pericardium.  That 
implies,  of  course,  very  marked  feebleness  in  the  heart's 
action.     Simple  dilatation  of  the  heart  to  the  extent  of 


DILATATION   OF  THE   HEART,  1 37 

becoming  a  disease  is   a  rare  occurrence.      I  have  met 
with  two  or  three  cases,  and  that  is  all. 

The  indications  of  it,  the  means  of  recognizing  it  during 
life,  are  both  physical  and  rational.  Among  the  physical 
signs  will  be  one  that  belongs  to  hypertrophy,  extended 
region  of  dulness.  The  lungs  will  be  pushed  away,  in 
the  same  way,  from  their  natural  position,  and  in  auscul- 
tation for  the  respiration  you  will  find  it  silent  over  the 
dilated  heart.  That  is,  the  lung  is  pushed  so  far  away 
that  the  sounds  of  respiration  will  not  be  brought  to  the 
ear  placed  in  the  middle  portion  of  the  pericardial  region. 
There  is  no  palpitation  proper.  It  frequently  happens, 
however,  that  the  patient  complains  of  palpitation.  His 
sensitiveness  is  increased  at  the  same  time  that  the  action 
of  the  heart  is  rendered  feebler ;  though  he  complain  of 
palpitation  you  put  your  hand  over  the  heart,  and  you 
can  scarcely  feel  it  beat.  In  one  case  that  I  saw  it  was 
remarkable  that  the  contraction  of  the  heart  was  in  a 
wave.  It  was  not  a  sudden  contraction  of  all  the  muscles 
of  the^  heart  at  the  same  moment,  but  the  contractile 
effort  seemed  to  pass  up  under  the  hand.  Beginning 
below  I  could  feel  the  wave  pass  the  length  of  my  hand. 
That  is,  so  far  as  it  was  applied  to  the  intercostal  spaces. 
I  could  not  feel  it,  of  course,  through  the  ribs,  but  the 
intercostal  spaces  being  thin,  as  I  exerted  some  pressure 
they  would  indicate  to  my  hand  the  kind  of  action  that 
was  taking  place  in  the  heart. 

A  feeble  beat  of  the  heart,  then,  with  an  increased 
region  of  dulness,  and  a  consideration  of  the  kind  of 
sound,  will  be  the  chief  physical  signs.  The  sounds  of 
the  heart  are  changed  in  relation  to  each  other ;  the  time 
is  changed,  or  the  rhythm,  as  it  is  called.  As  the  heart 
beats  naturally,  the  second  sound  follows  instantly  upon 
the  cessation  of  the  first,  and  then  there  is  a  period  of 
rest,  about  as  long  as  the  period  occupied  by  the  first  and 


138  DILATATION   OF  THE   HEART. 

second  sounds  together.  In  this  condition  you  are  very 
apt  to  have  the  motion  of  the  heart,  or  rather  the  sounds 
of  the  heart,  resembling  the  ticking  of  a  watch,  the  first 
and  second  sounds  at  even  distances  apart.  The  first 
sound  is  short,  scarcely  exceeding  in  duration  the  second. 
Tick,  tack ;  tick,  tack ;  in  about  that  relation. 

Then  the  appearance  of  the  patient  gives  a  marked 
indication  of  dilatation.  The  force  with  which  the  heart 
contracts  upon  the  blood  is  so  far  diminished  that  a  small 
quantity  is  sent  into  the  arteries  at  any  one  beat,  at  any 
one  time.  This  does  not  dilate  the  arteries,  does  not 
keep  them  of  their  natural  size.  They  are  apt  to  grow 
small  therefore.  I  referred  the  other  day  to  the  filling  of 
the  ventricle  during  the  period  of  rest  of  the  heart.  I 
perhaps  should  have  said  the  ventricle  has  no  power  of 
dilating  itself,  but  it  is  dilated  by  the  force  that  it  has 
impressed  upon  the  blood  when  it  went  out  from  the 
ventricle  into  the  arteries.  The  residual  force  of  the  cir- 
culation when  the  blood  returns  to  the  heart  is  really  the 
dilating  power.  In  that  sense  it  dilates  itself.  The  ve- 
nous power  is  considerable,  as  when  we  tie  the  arm  to 
bleed  a  man  the  force  of  the  current  is  such  as  to  throw 
the  blood  quite  a  considerable  distance  from  the  arm. 
This  force  is  not  all  exhausted  when  it  comes  to  the  right 
heart,  and  it  is  that  residual  force  impressed  upon  the 
circulation  by  the  contraction  of  the  left  side  that  opens 
the  right.  In  this  case  the  force  impressed  upon  the  blood 
going  out  of  the  right  side  of  the  heart  opens  the  left 
ventricle,  or  causes  the  left  auricle  to  fill,  and  this  is  really 
the  cause  of  the  filling  of  the  left  ventricle.  Now,  in  this 
dilated  heart,  you  have  a  very  feeble  force  impressed  upon 
the  blood  when  it  comes  out  of  either  ventricle.  It  will, 
of  course,  flow  into  the  opposite  ventricle  in  an  equally 
feeble  stream.  It  will  dilate  the  veins,  because  there  is 
not  force  enough  behind  to  empty  them,  and  you  get 


DILATATION   OF  THE   HEART.  1 39 

oedema  of  the  face,  of  the  feet,  and  of  the  surface  of  the 
body,  and  you  get  at  the  same  time  enlarged  veins ;  the 
blood  seems  to  rest  in  the  veins.  Of  course  it  does  not 
absolutely  rest,  but  the  current  is  slow. 

The  oppression  of  the  breathing  is  very  marked  in  these 
cases.  It  belongs  to  almost  every  form  of  disease  of  the 
heart,  but  is  developed  earlier,  and  is,  perhaps,  more 
severe  in  this  than  in  any  other,  and  that  depends  upon 
the  failing  force  with  which  the  blood  can  be  circulated 
through  the  lungs.  There  are  at  least  three  distinct 
causes  of  dyspnoea  besides  the  nervous  causes  that  would 
produce  the  same  thing.  One  is  an  over-charged  or  con- 
gested lung  or  lungs ;  another,  very  slow  circulation  of 
the  blood  through  the  lungs  ;  and  the  other,  some  physical 
obstacle  to  the  dilatation  of  the  lungs  by  the  air  entering 
them.  These  three  conditions  all  produce  dyspnoea  more 
or  less  severe,  and  why?  You  would  suppose  that, 
mechanically,  they  would  not  act  in  the  same  way. 
Mechanically,  they  do  not,  but  physiologically  they  do. 
They  each  one  interfere  with  the  aeration  of  the  blood. 
When  the  lungs  are  congested  the  blood  is  circulating 
slowly  through  them,  and  though  the  blood  that  is  in  the 
lungs  may  become  aerated  it  is  not  given  to  the  system 
with  sufficient  rapidity  to  answer  the  demands,  and  conse- 
quently a  sense  of  dyspnoea.  And,  then,  too,  when  the 
quantity  circulating  through  the  lungs  is  very  small  and 
the  current  slow,  there  is  not  enough  aeration  of  the  bulk 
of  the  circulating  blood,  and  there  is  dyspnoea.  Then, 
when  both  pleuritic  cavities  are  filled  with  serous  fluid, 
or  any  other  fluid,  and  the  lung  room  is  not  great  enough, 
there  is  not  space  for  very  much  aeration  of  blood,  and 
there  is  dyspnoea.  And  these  three  conditions  of  the 
lungs  explain  most  of  the  dyspnoeas  that  occur  with  the 
diseases  of  the  heart,  and  in  none  of  them  is  that  dyspnoea 
more  perceived,  more  apt  to  cause  sufl^ering,  than  in  this 


140  DILATATION  OF  THE   HEART. 

dilatation  of  the  heart.  These  are  the  leading  facts  by 
which  you  are  able  to  recognize  simple  dilatation  of  the 
heart,  if  you  should  happen  to  meet  it. 

With  reference  to  its  treatment  I  will  say  a  word.  There 
is  something  to  be  said  in  regard  to  this  that  does  not 
belong  to  all  forms  of  diseases  of  the  heart.  I  see  recom- 
mended in  some  of  the  text-books,  and  in  special  papers 
on  this  affection,  as  a  means  of  relief,  bleeding — bleeding 
from  the  arm.  Well,  I  will  tell  you  my  experience. 
When  I  was  house  physician  in  the  New  York  Hospital  a 
man  came  in  in  whom  we  recognized  dilatation  of  the 
heart,  and  it  was  in  that  particular  man  that  I  got  that 
wavy  motion  of  the  contractile  fibres  of  the  heart.  My 
principal,  seeing  how  much  he  suffered,  said,  bleed  him. 
I  looked  at  him  with  surprise,  and  said,  "  Doctor,  I  would 
not  dare  to  bleed  him.  He  cannot  lose  five  ounces  of 
blood  without  dying."  *'  Pooh,  pooh  !"  says  he.  **  If  you 
don't  like  to  bleed  him,  give  me  the  lancet."  He  tied  up 
the  arm  and  took  the  lancet.  I  was  accessory  in  holding 
the  bowl,  and  the  vein  was  opened.  The  man  bled  a 
little  spurt,  it  may  have  been  four  or  five,  possibly  six 
ounces,  and  rolled  over  on  the  bed — I  had  him  sit  on  the 
bed  on  purpose — rolled  over  on  the  bed,  and  breathed  no 
more.  Of  course  that  did  not  make  me  very  much  in 
love  with  bleeding  for  dilatation  of  the  heart.  And  yet, 
even  in  Niemeyer,  if  I  remember  right,  it  is  recommended, 
but,  I  suppose,  theoretically,  inasmuch  as  bleeding  does 
in  some  conditions  of  dyspnoea  give  relief.  But  I  do  not 
think  it  applicable  to  the  dyspnoea  which  arises  from 
dilatation  of  the  heart.  Well,  then,  there  is  very  little 
you  can  do.  The  man  cannot  take  any  exercise.  He 
would  drop  down  of  dyspnoea  if  he  were  to  make  any 
great  exertion.  He  may  walk  about  the  ward  a  little,  if 
he  is  in  a  hospital,  or  in  his  room,  if  at  home ;  but  that  is 
about  all  he  can  do.     He  cannot  go  up  stairs  and  can 


DILATATION   OF  THE  HEART.  I4I 

scarcely  go  down.  About  all  you  can  do  is  to  induce  him 
to  take  as  much  food  as  he  can  digest,  with  the  hope  of 
enriching  the  blood  a  little,  and  delaying  the  progress  of 
the  disease  ;  to  give  him  chalybeates,  which  will  help  in 
this  change  of  the  condition  of  the  blood,  almost  any  form 
of  iron  that  is  a  favorite  with  you ;  it  matters  very  little, 
for  they  all  go  to  about  the  same  thing ;  and  create  an 
active  condition  of  the  .kidneys  to  carry  off  the  oedema. 
This  latter  is  applicable  to  almost  all  the  forms  of  cardiac 
disease  where  dropsy  has  occurred.  I  shall  recur  to  the 
matter  of  diuretics  by  and  by. 

With  these  remarks  on  dilatation  of  the  heart,  we  will 
leave  that  subject  and  turn  to  another  conditionof  disease 
of  this  organ. 

Prof.  Maragliano*  gives  the  results  of  the  administra- 
tion of  strychnine  in  dilatation  of  the  heart  as  follows : 
I.  In  two  or  three  days  the  size  of  the  heart  was  reduced, 
and  in  five  or  six  days  very  considerable  dilatations  were 
caused  to  disappear.  2.  If  immediately  on  the  reduction 
in  the  size  of  the  heart  the  strychnine  were  withdrawn,  the 
dilatation  was  frequently  reproduced.  3.  The  daily  dose 
of  sulphate  of  strychnine  required  was  from  -^^  to  -^  of 
a  grain. 


*The  Medical  Record,  Jan.  27,  1883. 


142  FATTY  DEGENERATION   OF  THE   HEART. 


LECTURE  VII. 

FATTY  DEGENERATION  OF  THE  HEART. 

You  hear  a  great  deal  about  fatty  degeneration  of  the 
heart.  You  will  hear  a  great  deal  more  than  you  will 
see.  I  scarcely  ever  see  a  fat  man  advanced  somewhat 
in  years  who  has  trouble  with  the  heart,  that  the  attend- 
ing physician  does  not  say,  "Why,  doctor,  don't  you 
think  he  has  fatty  degeneration  of  the  heart?"  My 
reply  is  uniform,  "  I  cannot  diagnosticate  fatty  degenera- 
tion of  the  heart,  and  I  have  no  right  to  assume  it  in  any 
case  without  proof."  You  will  see  where  the  difificulty 
lies  pretty  soon.  Fatty  degeneration,  to  the  extent  of 
producing  real  disease,  is  quite  a  rare  occurrence ;  occur- 
ring, to  be  sure,  now  and  then,  but  in  comparing  it  with 
dilatation  and  hypertrophy  together,  it  hardly  bears  the 
relation  of  one  to  fifty. 

There  are  two  kinds  of  fatty  degeneration  of  this  organ. 
One  I  have«sometimes  designated  as  adipose  degeneration, 
or  adipose  deposit  upon  the  heart.  The  other  is  an 
integral  degeneration  of  the  muscle  of  the  heart  into  fat. 
The  latter  is  called,  commonly,  Quain's  degeneration,  as 
he  was  the  first  to  describe  it.  The  two  are  very  easily 
distinguished  by  the  appearance  after  death.  But  neither 
of  them  can  be  confidently  recognized  during  life.  The 
latter,  Quain's  disease,  you  will  be  more  likely  to  dis- 
tinguish than  the  other.  The  fatty  degeneration  of  the 
adipose  variety  is  merely  a  deposit  of  fat  upon  the  surface 
of  the  heart.  I  have  some  better  specimens  than  this 
which  I  can  show  you,  perhaps,  at  our  next  meeting, 
though  this  is  well  enough  marked  to  give  you  an  idea  of 


FATTY   DEGENERATION   OF  THE   HEART.  1 43 

what  is  meant  by  it.  Always  there  is  some  fat  upon  the 
exterior  of  the  heart  in  the  pericardium,  but  you  will 
observe  in  examining  this  specimen  that  here  it  has 
encroached  somewhat  upon  the  muscular  element  of  the 
organ.  The  whole  heartis  covered  with  a  more  or  less 
abundant  layer  of  fatty  tissue,  but  chiefly  upon  the  right 
side.  Well,  that  is  the  part  of  the  heart  that  is  most 
commonly  overloaded  with  this  fat.  You  take  a  portion 
of  this  fat  and  examine  it  under  the  microscope,  and  it 
will  present  exactly  the  same  appearance  as  adipose  tissue 
taken  from  any  portion  of  the  body — a  multitude  of  cells 
filled  with  oil.  It  is  a  healthy  fat  enough,  but  it  is  out  of 
place  here,  for  the  reason  that  as  it  becomes  abundant 
the  muscular  heart  becomes  weakened.  But  many  per- 
sons, no  doubt,  carry  this  condition  for  a  considerable 
time  without  knowing  it.  The  heart  performs  its  office 
with  fair  regularity  and  with  fair  force.  But  in  a  few 
instances  it  will  happen  that  the  fatty  encroachment  is 
unequal,  and  it  weakens  one  part  of  the  heart  more  than 
another;  as,  for  example,  the  septum  ventriculorum  may 
be  just  as  strong  as  it  ever  was,  while  the  wall  opposite 
is  weakened.  The  result  is  that  the  heart  sometimes  gives 
way  first  at  that  point ;  at  the  point  where  the  greatest 
weakness  of  its  muscular  tissue  is  it  bursts  itself.  I  will 
refer  to  that  again  a  little  further  along.  This  is  the 
heart,  then,  and  you  may  examine  it  and  see  what  it 
means.  The  fat  is  very  abundant  upon  the  base,  but 
that  does  not  do  so  much  harm  as  that  deposited  along 
the  course  of  the  ventricular  wall.  This  heart  is  also 
hypertrophied. 

I  told  you  the  heart  beats  with  perfect  regularity,  and 
that  it  is  not  enlarged  in  any  such  degree  as  that  you  can 
recognize  it  by  physical  signs.  Well,  then,  how  can  you 
recognize  it  at  all?  Well,  just  make  up  your  minds,  now» 
and  forever,  that  you  cannot  recognize  it,  except  after 


144  FATTY  DEGENERATION  OF  THE  HEART. 

death.  And  we  will  not  spend  a  great  deal  of  time  in 
talking  about  fatty  degeneration  of  the  heart,  when  you 
cannot  tell  what  is  the  matter  with  the  patient  when  he 
has  it. 

Now,  the  other  kind  is  altogether  different  in  its  effects 
upon  the  heart,  and  altogether  different  in  its  pathological 
aspect.  The  heart  muscle  is  a  striped  muscle.  It  has 
cross  markings,  lines  in  the  direction  of  its  length,  and 
lines  across  dividing  those  muscles,  as  the  muscles  of  the 
arm  and  leg,  and  all  the  voluntary  muscles  of  the  body 
are  divided  into  little  checks.  Well,  these  checks,  when 
Quain's  degeneration  occurs,  come  to  hold  first  a  little 
oil  globule.  A  muscular  element  seems  to  be  removed 
from  it.  The  place  of  the  muscular  element  is  taken  by 
oil  drops,  minute,  microscopic  drops.  I  can  show  you  a 
plate  the  next  time  that  will,  perhaps,  give  you  a  better 
idea  than  any  of  my  drawings,  but  you  may  get  some 
idea  of  it  from  this  drawing.  Well,  then,  this  sort  of 
heart  has  become  useless.  No,  not  quite,  because  this 
sort  of  degeneration  is  unequal  in  the  walls  of  the  cavities. 
It  will  be  here  marked,  and  at  another  place  scarcely 
noticeable.  The  result  of  this  production  of  oil  within  a 
muscle,  covering  the  sarcolemma,  is  to  change  the  color 
of  the  heart,  and  to  change  its  consistency.  Here,  for 
example,  are  three  specimens  of  this  kind  of  degeneration. 
This  one  is  not  so  very  much  softened.  It  seems  to  be 
small.  The  walls  of  the  heart  are  thin,  but  the  cavities 
are  not  dilated.  The  peculiar  color  that  the  oil  gives  to 
it  is  noticeably  yellow.  Here  is  another  which  is  soft  and 
yellow,  and  the  walls  of  the  heart  are  a  little  thinned,  but 
not  reduced  so  much  as  that  you  would  be  able  to 
recognize  it  during  life.  And  here  are  several  other  speci- 
mens which  you  will  examine  with  regard  to  color,  etc. 

In  regard  to  the  recognition  of  this  form  of  disease,  it 
is  more  nearly  possible  than  to   recognize   an   adipose 


FATTY  DEGENERATION  OF  THE  HEART.     I45 

deposit  Upon  the  exterior  of  the  heart.  For  example,  I 
was  called  to  see  a  lady,  not  quite  middle  aged,  in  whom 
there  was  marked  irregularity  in  the  action  of  the  heart. 
I  measured  its  size;  that  was  natural.  She  was  of  an  age 
that  would  hardly  admit  of  the  supposition  that  she  had 
bony  degeneration  of  the  heart  structure.  That  belongs 
to  advanced  age.  She  was  not  more  than  thirty,  or  per- 
haps thirty-five.  She  could  lie  down  flat  in  bed — that  is 
to  say,  she  could  lie  down  on  her  back  without  any  pillow 
or  bolster,  and  felt  better  in  that  position  than  with  her 
head  raised.  She  was  dizzy,  and  disposed  to  faint  when 
she  walked  about,  and  particularly  when  she  made  any 
exertion.  The  peculiar  irregularity — I  say  peculiar;  I  do 
not  know  that  that  is  the  proper  name — the  marked 
irregularity,  the  irregular  irregularity  in  her  heart  fixed 
on  my  mind  that  there  was  some  disease  of  it.  In  using 
that  expression,  irregular  irregularity,  I  ought,  perhaps,  to 
define  it.  When  a  heart  beats  on  for  five,  six,  or  seven 
minutes,  and  then  drops  a  beat,  that  is  an  irregularity; 
but  there  is  a  certain  degree  of  regularity  in  its  recurrence. 
You  may  count  a  certain  pulse,  and  find  that  the  sixth  is 
dropped  through  a  whole  minute.  But  when  there  comes 
a  kind  of  irregularity  that  you  cannot  describe,  when  the 
heart  beats  perhaps  rapidly  in  this  way  and  then  holds 
up,  beats  slowly,  and  then  directly  begins  with  a  sort  of 
fluttering  that  is  hardly  describable  in  words,  that  is  what 
I  mean  by  irregular  irregularity  as  contrasted  with  the 
regular  recurrence  of  certain  phenomena  in  the  action  of 
the  heart.  Well,  this  lady  had  that.  The  heart  beat  with 
an  irregularity  that  is  hard  to  describe.  Now,  it  will  be 
well  for  you  to  remember  that  that  belongs  to  some 
particular  disease  of  the  heart;  that  that  particular 
irregularity  that  you  cannot  well  describe  does  not  come 
of  mere  functional  disturbance,  but  is  always,  as  far  as 
my  memory  goes,  associated  with  a  change  of  some  kind 


146  FATTY  DEGENERATION   OF  THE   HEART. 

in  the  structure  of  the  heart  or  its  valves.  I  said  to  the 
doctor  who  called  me  in,  "  I  am  confident  there  is  some 
disease  of  the  heart  here,  but  I  cannot  tell  what  it  is." 
Had  I  known  the  fact  that  in  this  kind  of  degeneration 
it  is  not  uncommon  that  patients  can  lie  down  with  the 
head  low  in  bed,  and  feel  better  than  when  the  head  is 
raised,  I  might  perhaps  have  made  a  reasonable  conjecture. 
But  at  that  time  I  did  not  know  it — thirty  or  forty  years 
ago.  This  lady  died,  and  we  had  a  post-mortem  examina- 
tion, and  the  heart  I  think  is  one  of  these.  I  examined 
various  portions  of  it  under  the  microscope,  and  found 
the  kind  of  degeneration  that  I  have  been  trying  to 
describe  to  you,  more  or  less  in  all  parts  of  its  walls.  But 
it  was  very  marked,  more  marked  than  anywhere  else,  in 
the  fleshy  columns,  and  this,  perhaps,  was  one  reason  of 
the  marked  irregularity.  They  performed  their  office 
very  imperfectly,  and  by  sympathy  disordered  the  heart. 

This  kind  of  degeneration  is,  again,  of  rather  rare  oc- 
currence. It  may  occur  at  any  age.  It  may  occur  upon 
hypertrophied  and  dilated  hearts,  and  it  may  occur  upon 
hearts  that  are  perfectly  normal  in  size,  and  up  to  the 
time  of  its  occurrence  perform  their  function  properly. 

I  do  not  know  what  causes  Quain's  degeneration.  It. 
is  something  connected  with  the  nutrition,  the  nerves  of 
the  organ.  Persons  who  have  it  do  not  become  oedema- 
tous,  they  do  not  become  always  very  pale.  This  lady 
that  I  refer  to  was  pale  and  icteric,  but  I  did  not  refer 
the  icteric  element  to  the  heart,  unless,  perhaps,  the 
liver  was  deranged  by  imperfect  circulation  of  blood 
through  it. 

As  to  the  treatment  of  this  particular  form,  if  you 
make  it  out,  there  is  but  little.  A  rather  extraordinary 
recommendation  has  been  given,  however,  by  one  physi- 
cian of  some  authority,  and  that  is  to  advise  the  patient 
to  run  up-stairs.     I  think  it  would  kill  more  than  it  would 


FATTY  DEGENERATION   OF   THE   HEART.  I47 

cure.  The  idea  is  to  make  the  heart  active,  and  to  cause 
it  to  be  nourished  by  healthy  muscular  tissue  in  this  way. 
But  my  own  opinion  is  that  this  cannot  be  done.  The 
treatment  that  I  should  adopt,  and  have  recommended 
in  cases  where  this  disease  was  suspected,  is  of  an  en- 
tirely different  character.  It  is  aimed  at  causing  the  ab- 
sorption of  the  fatty  matter,  and  reduction  of  the  supply 
of  fat  in  the  body ;  for  example,  the  patients,  as  in  two 
or  three  other  forms  of  disease  that  depend  upon  fatty 
disorders  that  I  shall  describe  to  you  further  on,  are  di- 
rected to  take  moderate  exercise,  to  walk  upon  the  level 
ground,  or  upon  the  floor  of  the  house,  and  take,  accord- 
ing to  their  strength,  the  exercise  they  can  endure.  The 
second  element  of  the  treatment  is  to  exclude  from  the 
diet  all  fatty  food,  including  butter,  milk,  cream,  fat  of 
meats,  and  in  a  manner  all  fatty  food.  I  sometimes  al- 
low them  enough  of  milk  to  flavor  their  tea  or  coffee,  but 
nothing  beyond  that.  Only  lean  meat^,  and  the  vegeta- 
ble foods  that  contain  the  least  oily  matter.  Well,  the 
grains ;  perhaps  you  ask  whether  they  contain  oily  mat- 
ter; yes,  they  contain  oily  matter.  Wheat  contains 
about  three  per  cent.  Indian  meal  contains  about  ten 
per  cent — that  is  the  reason  it  fattens  the  hogs.  Then  I 
should  prescribe  food  made  from  wheaten  flour  rather 
than  from  Indian  meal.  And  next,  and  perhaps  the 
most  important  element  in  treatment,  is  to  administer 
the  bicarbonate  of  soda,  and  to  administer  it  in  as  large 
amount  as  will  be  borne,  and  that  fact  to  be  judged  of  by 
a  daily  examination  of  the  urine.  In  giving  alkalies  you 
are  to  bear  in  mind  that  some  of  them  have  the  power  of 
producing  calculi  in  the  kidneys  or  bladder,  but  there  is 
no  danger  of  their  producing  anything  of  this  sort  as  long 
as  the  urine  is  in  the  slightest  degree  acid.  Furnish  your 
patient,  then,  with  slips  of  litmus  paper,  to  be  kept  in  a 
convenient  place,  as  in  a  box  about  two  and  a  half  inches 


148  FATTY  DEGENERATION   OF  THE   HEART. 

long  and  an  inch  and  a  half  wide,  and  let  the  patient  take 
every  morning,  or  every  evening  (better  in  the  evening), 
one  of  the  papers  by  one  of  its  ends  and  dip  the  other  in 
the  water,  and  when  it  comes  out,  notice  whether  it  is  red 
or  purple.  If  it  is  purple  the  patient  is  taking  too  much 
soda ;  if  it  is  in  a  very  slight  degree  red,  that  is  all  right ;  if 
it  is  very  red,  he  is  not  taking  enough  ;  give  more.  And  in 
this  way,  from  day  to  day,  by  applying  the  test,  you  may 
give  what  will  be  safely  borne,  and  what  will  produce  most 
effect  upon  fatty  degeneration  of  any  kind  in  the  body  of 
the  patient.  I  do  not  know  from  experience  that  it  will 
do  any  good  in  this  kind  of  fatty  degeneration;  but  it 
does  so  much  good  in  other  kinds  of  fatty  degeneration 
that  I  deem  it  important  that  it  be  tried.  Of  course,  the 
most  nourishing  food  that  the  patient  can  take  is  to  be 
preferred ;  beef  and  mutton,  all  lean,  and  not  excluding 
chicken  and  fowls  of  various  sorts.  Any  good  whole- 
some meat  food,  is  better  than  vegetable  food  in  this 
case;  at  the  same  time  some  vegetable  food  may  be 
taken. 

Before  I  go  on  with  the  matter  of  rupture  of  the  heart 
it  is  probably  best  that  I  give  you  a  few  statistics  from 
different  authors  referring  to  the  frequency  of  disease  in 
the  several  valves  of  the  heart.  Here,  for  example,  in 
300  cases  of  endocarditis  in  the  adult,  297  were  on  the 
left  side,  32  on  the  right  side ;  268  were  confined  to  the 
left  side,  3  confined  to  the  right  side  ;  29  in  both.  (Taken 
from  statistics.)  In  the  foetus  and  newborn  child,  the 
evidence  of  endocarditis  was  in  192  cases  in  the  right 
side,  and  in  15  in  the  left.  Observe  the  very  marked 
disproportion  between  the  adult  record  and  the  infant 
record ;  192  in  the  right  side  in  the  infant  or  newborn,  15 
only  in  the  left ;  in  the  adult  297  out  of  300  cases  on  the 
left  side ;  but  29  of  these  were  on  both  sides  at  the  same 
time.     In  regard  to  the  particular  valve  that  is  most  liable 


FATTY  DEGENERATION   OF  THE   HEART.  1 49 

to  disease,  in  the  300  cases  255  were  in  the  mitral ;  a  por- 
tion of  these  were  in  the  aortic  also,  as  you  will  see  further 
on  ;  129  aortic  ;  in  the  tricuspid  valve,  29 ;  in  the  pulmonary 
valve,  3 ;  or  one  in  a  hundred.  Of  these  300,  159  were  of 
the  mitral  only  ;  40  were  of  the  aortic  valve  only  ;  3  of  the 
tricuspid  valve  only ;  and  none  of  the  pulmonary  valve 
only. 

Here  I  have  a  record  obtained  from  Bouillaud ;  and 
observe  it  is  in  hospital  practice,  for  children  in  Paris  are 
sent  to  a  hospital  separate  from  the  general  hospital.  He 
found  endocarditis  occur  in  55  per  cent  of  cases  of  articu- 
lar rheumatism.  Budd,  an  English  physician,  finds  it  in 
48.  Fuller,  in  23,  Wunderlich  and  Lebert,  in  23  per  cent 
in  a  hospital  for  adults. 

In  regard  to  embolism,  of  which  I  have  said  something 
to  you,  in  endocarditis  or  after  it,  different  parts  of  the 
body  are  the  seat  of  embolism,  or  parts  that  obstruct  the 
flowing  mass.  In  84  cases  that  were  observed  in  the  Berlin 
anatomical  museum,  57  were  of  the  kidneys,  but  not  of 
the  kidneys  alone ;  the  kidneys  were  the  seat  of  embolism 
in  57  out  of  the  84  cases.  But  these  emboli  are  not 
always  single ;  the  spleen  was  the  seat  of  the  same  accident 
in  39  of  the  cases;  the  brain  in  15  cases;  the  liver  and 
alimentary  canal  in  five  cases  only  out  of  84 ;  and  the 
vessels  of  the  skin  in  14.  Of  course,  in  several  of  these 
the  emboli  were  multiple ;  that  is,  different  organs  were 
affected  at  the  same  time. 


I50  RUPTURE  OF  THE  HEART. 


LECTURE  VIII. 

RUPTURE  OF  THE  HEART.  , 

Now,  with  reference  to  rupture  of  the  heart.  I  do  not 
beHeve  the  heart  is  ever  ruptured  when  it  is  in  a  sound 
condition.  You  have  just  seen  some  illustrations  of  rup- 
ture of  the  heart,  but  bear  in  mind  that  some  previous 
disease  may  have  existed  ;  it  may  be  there  was  what  they 
call  myocarditis,  a  form  of  disease  that  I  have  not  yet 
described  to  you.  That  produces,  as  you  will  see  when  I 
shall  describe  it,  a  weakening  of  the  muscles  here,  and 
makes  a  place  of  least  resistance,  and  a  place  that  is  liable 
to  give  way  under  the  power  of  other  portions  of  the 
heart.  The  specimens  that  you  are  examining  show  fatty 
degeneration,  or  rather  adipose  degeneration,  a  weaken- 
ing of  the  muscular  tissue,  for  fatty  tissue  has  little  con- 
sistency, gives  but  little  resistance  to  the  power  that  is 
acting  on  it.  Now,  if  you  had  the  means  of  determining 
in  what  particular  cases  this  adipose  degeneration  of  the 
heart  has  occurred,  you  might  anticipate  such  an  occur- 
rence, or  rather  you  might  conjecture  that  it  might  occur. 
And  that  is  about  as  far  as  you  can  go  in  the  diagnosis. 
I  told  you  when  we  were  last  together  that  we  have  no 
means  of  diagnosticating  fatty  degeneration  of  the  heart. 
You  observe  in  these  plates  that  the  organ  is  not  enlarged. 
There  is  no  valvular  sound  to  indicate  the  presence  of  any 
new  structure ;  therefore,  auscultation  amounts  to  noth- 
ing. The  heart  beats  naturally  and  easily  until  the  rupture 
comes.  It  may  come  during  some  period  of  considerable 
exertion,  and  the  first  you  know  of  it  is  sudden  death — 
and  then  you  do  not  know  what  is  the  cause  of  death 


RUPTURE   OF  THE   HEART.  151 

until  you  have  made  a  post-mortem  examination.  So 
that  speculation  in  this  direction  is  really  a  loss  of  time. 
You  can,  in  the  language  of  Goldsmith,  be  sure,  after  she 
is  dead,  that  her  last  disorder  was  mortal,  and  that  is 
about  all  you  can  say.  The  accident  may  surprise  you, 
then,  at  almost  any  time.  Still,  it  is  not  a  very  frequent 
occurrence.  When  it  occurs  from  a  weakening  of  the 
walls  of  the  heart,  of  th^  muscular  tissue  of  the  heart, 
from  previous  disease,  other  than  fatty  degeneration,  it 
will  be  likely  to  take  you  by  surprise  equally,  because 
there  is  no  murmur,  there  is  no  friction  sound,  there  is 
nothing  that  is  unnatural  in  the  action  of  the  heart,  unless 
perhaps,  occasionally  a  little  feebleness  which  you  can 
account  for  in  a  dozen  other  ways. 

When  it  follows  myocarditis  you  have  no  means  of 
anticipating  it.  It  is,  then,  practically  a  post-mortem 
disease  and  you  can  prescribe  no  treatment. 

Dr.  Ferguson  *  reported  to  the  N.  Y.  Pathological 
Society  a  rupture  of  the  heart  in  a  man  fifty  years  of  age. 
His  health  was  good  till  a  few  hours  before  his  death, 
when  he  suffered  from  dyspnoea.  He  died  in  the  water 
closet,  a  linear  rupture  in  the  anterior  wall  of  the  left  ven- 
tricle began  half  an  inch  above  the  apex  and  extended  up- 
ward three  quarters  of  an  inch.  There  was  an  increase  of 
the  fibrous  tissue  and  pus  in  the  muscular  wall  of  the 
ventricle. 

Also  another  instance  of  rupture  during  a  convulsion  in 
tetanus.  This  was  in  a  man  forty-four  years  of  age.  He 
had  a  laceration  of  the  left  hand,  and  three  weeks  after 
tetanus  began  on  the  anterior  of  the  heart  an  inch  to  the 
right  of  the  apex  there  was  a  circular  opening  of  one 
eighth  of  an  inch  in  the  right  ventricle,  the  wall  of  which 
at  this  point  was  a  line  in  thickness. 

*  The  Medical  Record,  Nov.  24,  1883. 


152  RUPTURE  OF  THE   HEART. 

Dr.  Da  Costa  ^  in  his  Toner  Lectures  relates  a  most  ex- 
traordinary breakage.  A  man  of  forty  years  had  parox- 
ysms of  severe  cardiac  pain  happening  at  irregular  intervals. 
They  were  attended  by  venous  pulsation.  This  pulsa- 
tion was  noticed  while  he  was  suffering  pain,  but  was 
marked  only  while  this  lasted,  or  just  before  or  after.  At 
this  autopsy  the  heart  was  found  to  be  enormously  hy- 
pertrophied  ;  one  of  the  papillary  muscles  of  the  tricuspid 
valve  was  torn  from  its  attachments  both  to  the  walls  of 
the  heart  and  to  the  tendinous  cord,  and  a  piece  was 
found  floating  in  the  pulmonary  artery.  The  right  auri- 
cle and  ventricle  formed  a  continuous  pouch  that  was 
filled  with  coagulum. 

Dr.  Coupiand  f  reported  a  case  of  spontaneous  rupture  in 
a  man  aged  sixty,  from  sudden  fright.  He  says  that  perhaps 
the  fullest  information  on  this  subject  is  given  by  Dr.  Quain 
in  his  Lumleian  Lectures,  Lancet,  1872  ;  I.  p.  460,  where  he 
states  that  in  yy  out  of  100  cases  there  was  fatty  degene- 
ration of  the  heart  walls  and  that  63  were  over  sixty  years 
of  age.  He  also  points  out  what  all  writers  have  noticed, 
that  the  exciting  cause  of  the  rupture  was  some  sudden 
mental  excitement  or  physical  exertion.  This  patient, 
till  the  accident  occurred,  had  had  no  symptoms  pointing 
to  heart  disease,  yet  the  coronary  arteries  were  advanced 
in  calcareous  degeneration,  and  there  was  considerable  adi- 
posity of  the  heart  wall  as  well  as  true  fatty  degeneration. 
This  case  resembled  the  majority  in  the  fact  that  the 
lesion  was  on  the  left  side.  In  most  cases  the  lesion  is  in 
the  anterior  wall,  either  in  the  region  of  the  apex  or  close 
to  the  septum.  In  this  case  it  is  on  the  posterior  wall,  at 
some  distance  from  the  septum  and  about  midway  be- 
tween the  apex  and  the  base.  According  to  Dr.  Quain  71 
deaths   in    100   were  sudden,    occurring   in  one  or   two 

*  Lecture  m.  f  Medical  News ^  Dec.  30,  1882. 


RUPTURE   OF   THE   HEART.  I  53 

minutes,  one  patient,  however,  lived  eight  days ;  i  five 
days ;  i  nine  days,  etc.  This  patient  Hved  forty-eight, 
and  the  inspection  disclosed  two  clots  in  the  pericardium 
of  different  ages,  and  between  the  two  effusions  he  rallied 
considerably. 

Dr.  Van  Santvoord*  reported  to  the  N.  Y.  Pathological 
Society  a  case  in  which  death  seemed  to  have  been 
hastened  by  entrance  of  air  into  the  pleural  cavity  in  the 
operation  of  tapping.  The  heart  was  markedly  hyper- 
trophied  and  dilated.  The  pericardium  was  thickened  and 
seemed  to  be  undergoing  atheromatous  change.  The 
valves  were  healthy.  The  microscopic  examination  of 
the  fibres  of  muscle  showed  no  degeneration  on  the  left 
side.  One  exhibited  a  marked  tendency  to  longitudinal 
spHtting  of  the  muscular  fibres.  On  the  right  side  the 
muscular  fibres  were  in  a  state  of  moderate  fatty  degene- 
ration. Why  there  was  heart  failure  was  not  shown  by 
the  examination. 

Dr.  Displatz  f  relates  a  case  in  which  a  sharp  fragment 
of  bone  lodged  in  the  oesophagus  about  half  way  down.  An 
abundant  hemorrhage  occurred  on  the  eighth  day  which 
ceased  spontaneously.  Thirty-six  hours  later  it  was  re- 
newed and  was  followed  by  death.  There  was  ulceration 
of  the  oesophagus  and  perforation  of  the  aorta  about  an 
inch  below  the  junction  of  the  transverse  and  descending 
portions. 

Dr.  Wm.  Axford  if  reports  two  cases,  one  in  a  boy  aged 
16,  the  other  in  a  boy  of  15  years.  The  first  *'  while  car- 
rying a  heavy  weight  made  a  sudden  and  great  muscular 
effort.  Soon  he  complained  of  considerable  pain  in  the 
centre  of  the  sternum,  also  of  uncomfortable  feeling  in  the 
left  arm  ;  expectorated  some  blood  ;  short  dry  cough."     A 

*  Medical  Record,  March,  17,  1883. 
flbid.,  June  2,   1883. 
J  Ibid.,  March"  24,  1883. 


154  RUPTURE   OF  THE   HEART. 

time  after  his  pulse  was  lOO,  temperature  g7i°,  respiration 
26,  irregular.  There  was  an  aortic  regurgitant  mur- 
mur. Since  this  accident  the  boy  has  not  been  able  to 
do  any  hard  work,  but  earns  his  living  by  bookkeeping. 

In  this  second  case,  a  boy  in  good  health  made  a  sud- 
den and  violent  effort  to  control  horses  he  was  driving, 
and  immediately  felt  pain  in  the  region  of  the  heart  and 
said  he  could  not  get  his  breath  for  several  days.  Syn- 
cope and  a  sense  of  impending  suffocation  followed  mental 
excitement  or  muscular  effort  often,  and  up  to  the  time 
of  the  report  he  could  not  make  any  physical  exertion. 
All  who  saw  him  found  mitral  regurgitation. 

Dr.  Axford  adds  that  Corvisart  was  the  first  to  point 
out  the  fact  that  this  injury  was  possible  and  that  it  could 
by  caused  by  muscular  exertion.  Dr.  Peacock,  he  says,  in 
1865,  had  collected  seventeen  cases,  four  of  which  came 
under  his  own  observation.  The  valves  injured  were : 
the  aortic  ten  ;  the  mitral  four ;  the  tricuspid  three. 

Dr.  Brenner"^  reports  the  following :  A  woman  fifty- 
five  years  old,  had  repeated  hemorrhages  from  the  stom- 
ach and  died  in  consequence.  She  had  had  pleurisy  of 
the  left  side  six  weeks  previously.  The  left  lung  was 
retracted  and  closely  adherent  to  the  diaphragm.  The 
two  surfaces  of  the  pericardium  along  the  left  border  of 
the  heart  were  closely  adherent  and  the  dilated  stomach 
along  the  lesser  curvature  to  the  diaphragm.  About  two 
inches  from  the  cardiac  orifice  on  the  lesser  curvature  was 
a  round  ulcer  almost  as  large  as  the  palm  of  the  hand,  at 
the  edges  of  which  were  seen  gaping  coronary  vessels. 
At  the  bottom  of  the  ulcer  was  a  sinus  communicating 
directly  with  the  cavity  of  the  left  ventricle  through  an 
opening  in  the  endocardium  the  size  of  a  pea.  There 
were  no  serious  cardiac  disturbances  during  life.     "  The 

*  The  Medical  Record,  Oct.  7,  1883,     ^ 


RUPTURE   OF  THE   HEART.  1 55 

hemorrhage  was  from  the  coronary  arteries  of  the  stomach 
and  not  from  the  heart." 

In  two  cases  of  perforation  of  the  left  ventricle  of  the 
heart  by  gastric  ulcer  Oser,*  at  autopsy,  discovered  a 
round  ulcer  of  the  stomach  which  had  penetrated  the 
left  ventricle  of  the  heart.  The  communication  between 
the  organs  was  through  a  long  narrow  canal.  No  air 
was  found  in  the  heart  or  vessels.  The  woman  was 
seventy-one  years  old.  The  perforation  was  indicated 
three  days  before  death  by  the  vomiting  of  bright  arterial 
blood  and  by  tarry  stools. 

Brenner  had  just  published  a  similar  case  occurring  in 
a  woman  55  years  old.  She  had  had  for  years  attacks  of 
cardiac  pain,  occasionally  attended  by  vomiting.  A  few 
days  before  death  she  vomited  blood,  had  black  tarry 
stools  and  great  cardiac  distress.  A  circular  ulcer  was 
found  in  the  lesser  curvature  of  the  stomach,  which  com- 
municated with  an  opening  in  the  wall  of  the  left  ventricle. 

Dr.  Blockf  of  Dantzig  has  been  trying  to  show  that  the 
heart  when  wounded  can  be  sutured  and  life  saved  by 
experiments  on  dogs  and  rabbits.  Four  experiments  with 
rabbits  showed  that  both  thoracic  and  pericardial  cavities 
can  be  opened  for  a  short  time  with  impunity.  An  open- 
ing of  the  right  and  left  ventricle  as  well  as  an  entire  com- 
pression of  the  heart,  for  the  application  of  suture,  can  also 
be  supported  by  animals  for  a  few  minutes,  and  he  pre- 
sented a  dog  in  good  health  in  which  there  had  been  a 
wound  of  the  cardiac  muscle  with  opening  and  suture  of 
the  three  thoracic  cavities. 

In  order  to  prevent  the  escape  of  blood  in  the  applica- 
tion of  the  sutures  the  heart  is  to  be  seized  at  the  apex 
and  drawn  forward  until  pulsation  and  respiration  cease 

*  Am.  your,  of  Med.  Sci.,  April,  1882. 
t  Ibid.,  Jan.,  1883. 


156         FIBROUS  DEGENERATION  OF  THE  HEART. 

(the  animal  not  being  necessarily  killed  by  the  procedure) 
or  the  traction  on  the  heart  can  be  made  only  sufficiently 
strong  to  arrest  the  escape  of  blood  from  the  wound. 
The  wound  can  then  be  ligatured  or  sutured. 


LECTURE   IX. 

FIBROUS   DEGENERATION   OF   THE   HEART. 

Now,  then,  I  have  something  to  say  to  you  about  the 
heart  clot.  No,  not  yet ;  fibrous  degeneration  of  the 
heart  comes  before  that,  because  it  is  of  the  heart  struc- 
ture itself.  Dr.  Quain,  who  gave  us  our  first  ideas  of 
fatty  degeneration  of  the  muscular  fibres  of  the  heart,  a 
few  years  ago,  described  what  he  regarded  as  hypertrophy 
of  the  heart  arising  from  increase  of  its  connective  tissue. 
He  called  it  fibrous  hypertrophy.  I  have  been,  from  the 
time  he  made  this  statement,  a  little  skeptical  in  regard 
to  the  correctness  of  his  opinion.  But  during  the  present 
winter  I  have  examined  by  the  microscope  some  speci- 
mens that  are  unquestionably  of  the  character  that  he 
described,  and  a  little  further  on,  when  you  have  fewer 
specimicns  to  handle,  I  will  show  you  some  specimens 
under  the  microscope  that  will  illustrate  this  form  of  dis- 
ease. In  specimens  in  my  possession  newly  formed 
fibrous  tissue  or  connective  tissue  is  seen  by  the  micro- 
scope in  great  abundance.  In  parts  it  is  laid  in  between 
the  muscular  fibres  of  the  organ.  This  new  material, 
thus  deposited,  may  have  the  width  of  one  muscular 
fibre,  or  that  of  ten  or  twelve  and  more.  In  other  parts 
it  cuts  across  these  fibres,  causing  their  absorption  so  far 
as  the  new  deposit  extends.  Then  again  it  is  laid  in  in- 
termittently, leaving  a  short  fragment  of  a  muscular  fibre 


FIBROUS   DEGENERATION   OF   THE   HEART.  1 57 

isolated,  and  then  another  and  another,  all  lying  in  the 
same  line,  contiguous  fibres  all  broken  up  in  the  same 
way  over  a  space  which  may  fill  two  fields  of  the  micro- 
scope. Thus,  in  the  field,  which  seems  to  be  four  or  five 
inches  in  diameter,  fragments  of  muscle,  appearing  half 
an  inch  long,  broken  by  a  layer  of  connective  tissue  and 
disappearing,  reappear  at  variable  distances,  presenting 
another  semi-fragment,'  and  so  the  field  is  checkered, 
the  connective  tissue  showing  its  peculiar  cells,  and  the 
muscular  fragments  their  double  striation.  Thus  in  cer- 
tain parts  of  the  heart  the  muscular  fibres  are  broken  up 
and  their  continuous  action  wholly  lost.  It  seems  that  the 
connective  tissue  can  take  on  hypertrophy  by  itself  alone. 
The  quantity  of  it  that  may  be  found  upon  the  spleen, 
sometimes  called  a  cicatrix,  is  enormous,  and  it  is  perfectly 
well  formed  connective  tissue,  with  the  fibres  and  with  the 
nuclei,  and  it  may  be  half  an  inch  in  thickness.  The  con- 
nective tissue  in  the  liver  is  multiplied  very  much  in  certain 
forms  of  disease,  as  is  also  the  connective  tissue  in  other 
parts  of  the  body  occasionally.  But  in  the  heart  it  seems 
to  have  had  but  a  recent  discovery.  All  the  hypertro- 
phies that  have  been  noticed  have  been  deemed  to  be 
hypertrophy  of  the  muscular  tissue  only.  As  to  the 
mode  in  which  this  particular  form  of  disease  presents 
itself  under  the  microscope,  when  you  make  a  section  of 
an  enlarged  heart,  you  follow  the  muscular  tissue  a  certain 
distance,  and  then  it  breaks  up,  and  in  the  place  of  it  you 
find  connective  tissue,  and  the  connective  tissue  may  be 
wide  enough  to  reach  the  whole  breadth  of  the  field  of  the 
microscope,  and  no  muscular  tissue  in  it.  But  you  see 
muscular  fibres  ending,  one  here  and  another  there,  then 
gone,  and  then  by  and  by  they  will  be  observed  again — 
that  is,  at  a  little  distance  from  where  they  disappeared. 
It  seems  then  to  destroy  the  muscular  tissue,  when  the 
hypertrophy  of  the  connective  tissue  is  marked.     But  fre^ 


T5§         FIBROUS  DEGENERATION   OF  THE  HEART. 

quently  it  seems  to  occur  without  being  really  a  disorder. 
There  is  always  between  the  layers  of  muscular  fibre  of  the 
heart  some  connective  tissue.  The  bundles  are  separated  by 
something  more  than  a  myolemma,  sarcolemma,  or  what- 
ever name  you  may  give  it ;  some  real  connective  tissue 
thrown  in  between  the  sarcolemma  of  the  different 
bundles  of  fibres.  You  see  that  in  passing  a  micro- 
scope over  a  thin  section  of  the  heart  in  almost  any 
instance.  Well,  this  increases  in  quantity,  of  course 
increases  in  thickness,  and  by  just  so  much  as  it  in- 
creases beyond  a  certain  point  it  seems  to  diminish  the 
muscular  fibres  by  compression ;  that  is,  causes  their  ab- 
sorption and  removal.  When,  then,  this  form  of  disease 
presents  itself  in  any  decided  manner,  you  can  easily 
comprehend  that  you  will  have  an  enlarged  heart  with 
diminished  power ;  this  deposit  is  for  the  most  part  in 
lieu  of,  or  a  substitution  for,  the  muscular  fibres,  and  as  it 
has  no  contractile  force,  upon  itself,  it  will  only  diminish 
the  strength  of  the  heart.  I  do  not  know  that  we  are 
advanced  far  enough  in  our  knowledge  of  disease  to  dis- 
tinguish between  fibrous  hypertrophy  and  muscular 
hypertrophy ;  it  requires  some  further  observation ;  but 
it  is  important  that  you  know  that  there  is  such  a  thing 
as  fibrous  degeneration  of  the  heart  with  increase  in  size. 
It  is  a  matter  that  is  open  to  study  yet.  The  study  has 
not  been  pursued  far  enough  to  enable  us  to  lay  down 
rules  and  principles  in  regard  to  it. 


HEART  CLOTS.  1 59 


LECTURE  X. 

HEART   CLOTS. 

Now,  then,  we  come  to  heart  clot.  I  give  a  little  time 
to  the  matter  in  the  lectures,  as  I  used  to  receive  from 
the  graduates  of  the  college  long  letters  in  regard  to  it. 
I  remember  one,  four  sheets  of  foolscap,  written  on  each 
side  of  the  page,  describing  a  something  that  was  terri- 
ble. A  clot  had  formed  in  the  heart,  and  extended  out 
in  the  vessels  about  as  far  as  the  examiners  could  pursue 
them,  and  it  was  wonderful  that  a  man  could  live  with 
such  a  thing  in  his  heart ;  well,  he  did  not.  All  that 
formed  after  he  died. 

A  distinguished  physician  of  Philadelphia  wrote  a  book 
on  the  frequent  occurrence  of  ante-mortem  heart  clot. 
He  thought  they  were  of  very  frequent  occurrence.  I  do 
not  believe  that.  That  clots  can  form  in  the  heart  pre- 
vious to  death,  and  may  cause  death,  I  fully  believe,  but 
the  occurrence  is  rare.  I  will  make  you  understand  that, 
I  think,  before  we  get  through.  Now,  to  distinguish 
between  the  clot  that  is  formed  before  death  and  one 
that  is  formed  after,  there  are  two  or  three  rules  that 
will  be  diagnostic.  You  come  to  a  heart,  the  left  ventricle 
of  which  is  filled  with  coagulated  blood,  and  the  blood  runs 
on  out  through  the  aorta,  and  you  can  follow  it  to  some 
of  the  ramifications  of  the  large  vessels ;  or  it  forms  in 
the  right  side,  and  extends  through  the  pulmonary  artery 
into  even  minute  branches  of  the  pulmonary  vessels,  and 
it  does  really  look  like  a  very  formidable  thing,  and  a  per- 
son who  does  not  understand  it  would  assume  that  it 
was  as  bad  as  violent  death.     Now,  then,  if  a  clot  form  in 


l6o  HEART  CLOTS. 

the  heart  before  the  heart  ceases  to  beat,  it  can  never  be 
attached  to  all  the  periphery  of  the  heart.  If  the  heart 
has  ever  beaten  upon  the  clot  that  has  formed  in  it, 
the  contraction  that  must  follow,  if  life  continues,  will 
separate  the  clot  from  all  the  external  walls,  from  every- 
thing except  the  septum  ventriculorum ;  and  when  clots 
are  found  in  the  heart  that  have  been  formed  during  life, 
they  are  always  attached  to  the  septum,  usually  to  the 
lower  part  of  the  septum,  where  are  the  greatest  number 
of  pectinean  muscles.  The  very  act  of  contraction  must 
separate  it.  If  you  will  think  of  it  for  a  moment,  you 
will  see  it  cannot  be  otherwise. 

These  clots  are  of  two  colors,  buff  and  black.  The  buff 
is  uppermost  with  reference  to  the  position  of  the  body 
after  death ;  the  dark  colored  is  the  dependent  portion. 
Now  what  is  that  buffy  coat  ?  Exactly  what  takes  place 
in  the  blood  when  withdrawn  into  a  bowl  and  allowed  to 
stand.  The  upper  layer  has  been  formed  by  the  sinking 
of  the  blood  corpuscles  into  the  deeper  layer,  and  that 
takes  time.  There  is  not  time  between  two  heart  beats 
for  anything  of  that  kind  to  take  place,  and  the  occur- 
rence of  a  clot  with  a  buffy  portion  and  a  dark  portion  is 
conclusive  evidence  that  the  coagulation  took  place  after 
death.  The  heart  was  full ;  it  died  expanded,  and  the 
coagulation  took  place  in  a  manner  that  would  require 
several  minutes  to  form  it,  perhaps  an  hour  or  two.  The 
blood  does  not  coagulate  quickly  within  the  body.  It 
has  been  estimated  that  it  requires  about  six  hours  for 
the  blood  to  become  firmly  coagulated  after  death. 
Sometimes  it  takes  a  much  longer  time  than  that,  but  a 
quick  coagulation  does  not  take  place.  As  the  blood- 
corpuscles  are  a  little  heavier  under  most  circumstances 
than  the  fluid  portion  of  the  blood,  their  specific  gravity 
being  a  Httle  greater,  they  have  time  to  sink  to  the  deeper 
portions  of  the  pool  of  blood,  and  allow  the  surface  to 


HEART   CLOTS.  l6l 

coagulate  with  a  buffy  coat,  a  yellowish,  semi-transparent 
substance.  That,  then,  is  conclusive  evidence  against  the 
chances  of  ante-mortem  heart  clot. 

It  has  been  assumed  frequently  enough  that  the  in- 
dentation of  the  clot  at  the  point  where  the  valves  are 
placed  is  evidence  of  an  impression  made  upon  it  by  the 
action  of  the  heart  during  life.  But  this  is  altogether 
another  thing.  When  death  takes  place  and  the  heart 
ceases  to  send  a  current  of  blood  through  the  aorta,  the 
upper  portion  of  the  valve  of  the  aorta  falls  downward 
of  its  own  weight  into  the  blood  ;  the  lateral  ones  fall  a 
little  but  not  so  much.  The  anterior  is  the  point  where 
quite  an  indentation  in  the  coagulum  has  been  noticed ; 
it  falls  into  the  fluid  blood,  and  when  the  coagulation 
takes  place,  it  will  take  place  about  that  valve  that  hangs 
in  it,  and  of  course  it  will  leave  an  indentation  in  it.  So 
far  from  being  an  evidence  of  ante-mortem  clot,  that 
particular  thing  is  evidence  that  it  formed  after  death. 
Almost  all  the  clots  that  are  found  after  death  are 
formed  after  death  in  the  heart  and  great  vessels. 

If  the  clot  has  formed  before  death,  and  the  heart  has 
beaten  upon  it,  it  has  become  compressed  and  will  be 
found  attached  to  the  lower  part  of  the  septum  ventricu- 
lorum  and  not  to  the  walls  of  the  heart,  unless  it  be  the 
very  apex.  Clots  are  formed  in  the  heart.  Here  is  a 
figure  of  one,  and  you  observe  it  is  rather  crab-like  in 
form  ;  it  has  several  legs. 

Cardiac  Thrombosis  in  Acute  Disease. — Dr.  Goodridge  * 
bases  his  opinion  on  three  cases  in  which  death  occurred 
with  greater  or  less  degree  of  suddenness  and  with  attend- 
ant symptoms  of  dyspnoea,  thoracic  oppression,  rapidly 
diminishing  heart  power,  and  a  sense  of  impending  disso- 
lution.    In  these  cases  there  were  found  firm  decolorized 

*  N,  Y.  Med.  Journal,  Oct.  20,  1883. 


l62  HEART   CLOTS. 

coagula,  occupying  in  one  case  the  left  ventricle  and  the 
beginning  of  the  aorta;  in  another,  extending  from  the 
right  ventricle  into  the  pulmonary  artery,  and  in  the  last 
blocking  up  the  right  auricle  and  the  superior  vena  cava. 
In  the  last  case  the  fibrous  coagulum  was  distinctly  lam- 
inated, and  the  symptoms  pointed  to  a  progressively  in- 
creasing interference  with  the  function  of  the  right  heart. 
At  a  meeting  of  the  section  in  Practice  of  the  Academy 
of  Medicine,  Dr.  J.  Lewis  Smith*  defended  the  opinion 
always  taught  from  this  chair  since  I  have  occupied  it, 
that  the  white  clots  and  those  that  have  an  upper  layer 
of  white  and  a  deeper  one  of  very  dark  color  are  always 
and  necessarily  of  post-mortem  origin.  He  brought  into 
his  argument  a  very  important  case.  He  had  in  the  hos- 
pital a  man  whose  symptoms  led  him  to  suppose  that  the 
right  heart  was  overloaded  with  blood.  Feehng  that 
benefit  might  follow  the  withdrawal  of  some  of  this  blood 
he  introduced  a  hypodermic  syringe  and  removed  a  cer- 
tain quantity.  This  blood  was  of  dark  color  and  perfectly 
fluid.  The  heart  had  ceased  beating  before  the  syringe 
was  introduced,*  and  cardiac  action  did  not  follow.  Dr. 
Janeway  then  injected  a  solution  of  carbonate  of  am-' 
monia  into  the  same  cavity,  but  it  also  failed  to  excite  the 
heart  to  action.  At  the  autopsy  there  was  found  a  firm 
white  clot  entangled  in  the  chordae  tendiniae  and  columnae 
carneae  and  not  any  dark  fluid.  Immediately  after  the 
heart  ceased  to  beat,  the  right  cavity  contained  fluid  dark 
blood.  At  the  autopsy  there  was  no  fluid  dark  blood  in 
the  same  cavity,  but  a  firm  white  clot  entangled,  as  de- 
scribed. 


*The  Medical  Record,  Jan.  13,  1883. 


VALVULAR  DISEASE.  163 


LECTURE  XI. 

VALVULAR   DISEASE. 

It  is  necessary  to  refer  to  other  causes  of  valvular  dis- 
eases. The  most  common  is  the  deposit  of  that  substance 
that  looks  like  mucine,  that'I  have  described  to  you.  Its 
organization  and  contraction,  producing  what  I  have 
already  denominated  the  shortening,  thickening,  and  stiff- 
ening of  the  valve.  These  same  results  may  be  obtained 
when  other  agents  are  at  work.  One  of  the  things  that 
operates  most  actively  after  inflammation  is  atheroma. 
Atheroma  originally  meant  an  abscess,  but  it  has  come 
to  mean,  in  these  later  years,  a  particular  deposit  that  is 
confined  almost  entirely  to  the  heart  and  arteries,  much 
more  common  in  the  arteries  than  in  the  heart  itself,  but 
in  the  valves  not  infrequently  met  with.  This  atheroma 
you  can  form  an  idea  of  by  the  specimens  which  I  can 
exhibit  to  you.  When  you  first  find  atheroma  in  the 
dead  body  it  is  almost  always  of  a  yellow  color,  or  a  faint 
yellow  color.  Here  it  is  white.  It  has  been  bleached  by 
alcohol,  in  which  the  specimen  I  show  you  has  been  kept. 
If  you  handle  the  specimen  you  will  find  that  at  different 
parts  it  is  of  uneven  thickness.  There  are  little  warty, 
flattened  eminences  upon  the  whole  circumference  of  it, 
and  at  the  edge  you  can  get  an  idea  of  its  thickness. 
Here  is  another  artery  that  is,  to  a  certain  extent,  warty, 
exhibiting  the  same  thing,  lacking  the  yellow  color  which 
belongs  to  it  when  it  is  first  seen.  You  observe  it  runs 
up  the  artery  a  considerable  distance,  that  is  the  aorta. 
You  observe,  too,  that  it  has  narrowed  the  openings  of 
the  three  arteries  that  are  given  off  from  the  aorta.    Here 


164  VALVULAR  DISEASE. 

is  an  interesting  specimen  of  an  atheromatous  deposit  in 
a  valve  and  not  in  the  artery,  or  if  any,  very  little.  The 
valve  has  undergone  one  of  the  changes  that  I  will  describe 
to  you  directly,  and  it  has  ulcerated  a  hole  through  the 
valve.  Not  only  that,  but  it  seems  to  have  been  deposited 
upon  the  substance  of  the  heart,  probably  not  in  the  sub- 
stance, and  an  opening  has  been  made  at  the  same  time 
from  one  ventricle  to  the  other.  A  broom  straw  has 
been  passed  through  the  whole,  from  one  ventricle  to  the 
other,  and  you  will  observe  what  an  ulcerated  and  damaged 
condition  this  valve  is  in.  Here  are  a  number  of  other 
specimens  which  you  will  examine. 

Now,  then,  the  first  question  that  comes  is,  what  is  this — 
this  atheromatous  matter?  Well,  it  is  an  effusion  on  the 
outside  of  the  inner  lining  of  the  artery ;  the  intima,  as 
it  is  the  fashion  to  call  it  now.  It  lies  outside  of  the  lin- 
ing membrane  of  the  artery.  It  is  to  a  certain  extent 
infiltrated  into  the  fibrous  tissue  of  the  artery,  but  it  is 
much  more  commonly  found  just  between  the  lining 
membrane  of  the  artery  and  the  fibrinous  layer,  called 
media  in  these  later  days.  Between  the  intima  and  the 
media,  then,  is  to  be  found  this  deposit.  And  it  is  con- 
stituted sometimes  of  a  material  very  much  resembling 
that  which  I  have  described  to  you  as  thickening  the  valves 
in  endocarditis,  a  sort  of  mucous  matter,  and  that  is  thick 
set  with  cells  that  do  not  grow,  do  not  develop  themselves 
according  to  the  rules  of  cell  growth  in  other  parts  of  the 
body,  but  become  attached  to  each  other  on  almost  any 
point  where  they  may  touch,  and  thus  form  a  kind  of 
tissue.  Then  that  is  pretty  fully  infiltrated  with  little 
globules  of  oil,  and  occasionally  a  few  fibres  are  formed 
by  the  coalescence  of  these  cells,  but  they  possess  very 
little  power  of  permanent  life.  And  the  result  of  this  is 
a  pretty  early  change  in  their  constitution.  The  cells 
disintegrate,  and  oily  globules  seem  to  take  their  place. 


VALVULAR   DISEASE.  165 

The  fibres  gradually  disappear,  being  broken  down  into 
granules,  and  soon  the  means  of  organization  have  passed. 
This  takes  place  very  soon,  that  is  in  a  few  months,  or  a 
year  or  two  at  most.  The  result  of  the  breaking  down  of 
the  structure  is  a  softening,  and  you  can  sometimes  find 
these  little  deposits  of  soft  material,  looking  exactly  like 
pus,  except  a  little  yellow.  Put  them  under  your  micro- 
scope and  you  will  find'  that  there  are  no  pus  globules  in 
them.  The  result  of  this  is,  sometimes,  to  leave  an  ulcer 
on  the  artery,  or,  as  in  the  specimen  you  are  examining,  in 
the  valves,  and  more  frequently  at  the  base  of  the  valves 
than  at  any  other  part  of  them.  A  weakening  of  the 
structure  is  therefore  produced,  without  softening.  This 
atheromatous  matter  has  no  strength  and  it  has  no  elas- 
ticity. It  cannot  replace  in  function,  as  it  replaces  in 
position,  the  fibrous  tissue  of  the  artery.  The  wall  grows 
weak  by  the  deposit  of  this  matter  in  it,  therefore,  and 
you  may  start,  with  regard  to  aneurism,  with  this  asser- 
tion, that  aneurisms  in  the  human  body  do  not  occur 
except  by  violence  or  by  the  weakening  of  the  coats  of 
the  artery  or  through  an  atheromatous  deposit. 

An  aneurism  in  any  of  the  large  trunks  of  the  circulatory 
system  will  not  occur  without  atheroma  ;  the  artery  must 
be  weakened  before  it  will  yield,  and  weakening  is  always 
effcted  by  atheroma  of  the  artery.  You  may  search  for  twen- 
ty years  among  aneurisms,  and  you  will  not  find  a  single  one 
that  has  occurred  in  a  sound  artery.  Even  those  minute 
ones  that  have  been  lately  described  in  the  brain  circula- 
tion have  for  their  base  atheromatous  weakening  of  the 
arteries  of  the  brain.  Well,  this  is  a  pretty  grave  matter, 
then,  for  it  is  the  parent  of  aneurism  ;  it  also  produces  the 
weakening  that  precedes  what  is  called  dissecting  aneu- 
rism. The  artery  may  break  partly  in  two,  the  inner  lay- 
ers may  be  broken,  and  the  blood  may  find  its  way  be- 
tween the  layers  of  the  artery  for  a  very  considerable  dis- 


1 66  VALVULAR   DISEASE. 

tance.     This,  however,  I  believe  only  occurs  in  the  large 
arteries,  the  thoracic  and  the  abdominal.     I  do  not  know 
but  it  occurs  in  the  iliac  sometimes.     That,  also,  I  say, 
has  its  origin  in  the  weakening  of  the  arterial  coats  by 
this  atheromatous  deposit.    This  is  one  of  the  courses  that 
an  atheroma  pursues  when  it  is  once  deposited  in  the  ves- 
sels.    Another  is  interesting  perhaps,  not  to  say  impor- 
tant, in  its  bearing.     The  atheromatous  matter  is  broken 
down  very  much  in  the  same  way  as  I  have  described  to 
you,  but  more  gradually,  and  the  fat  which  seems  to  be 
taken  up  by  the  circulatory  vessels,  and  deposited  in  the 
place  of  the  atheromatous  matter  is  bony  structure,  bony 
scales.     Such  a  specimen  as  that  I  will  try  to  show  you 
the  next  time  we  come  together,  in  which  the  whole  ar- 
tery has  been  converted  into  scales,  a  multiplication  of 
scales,  some  of  w^hich  have  a  real  bony  structure — have 
the  lacunae  and  the  canaliculi ;    and   some  of  which  are 
mere  calcareous  accretions,  without  anything  which  dis- 
tinguishes bone.     These  render  the  artery  inelastic,  and 
so  interfere  with  the  circulation.     As  I  have  already  told 
you,  the  heart  sends  the  blood  into  the  artery  and  dilates 
it,  and  the  artery,  by  its  natural  contractile  power,  propa- 
gates or  continues  the  action  produced  by  the  heart,  car- 
rying the  blood  forward  in  the  circulation.     But  in  an  ar- 
tery that  has  been  deformed  in  this  way  the  elasticity  is 
gone.     Hence,  in  such  cases  it  is  not  uncommon  that  hy- 
pertrophy occurs.     There  is  another  evil  that  may  come 
of  these  bony  scales ;  they  are  sharp  at  the  edge ;  they 
are  thin.     I  say  sharp  ;  they  have  almost  a  cutting  edge  ; 
and  the  gradual  action  of  the  artery,  or  so  much  as  is 
left  of  it,  may  cut  through  the  inner  lining  and  let  one  of 
the  sharp  edges  stand  out  like  the  edge  of  a  nail,  or  the 
end  of  a  nail  rather,  and  on  this  may  form  the  accretions 
of  fibrine,  the  coagulations  of  fibrine,  or  vegetations,  and 
these,  in  their  turn,  may  wash  off  and  make  emboli.     In 


VALVULAR   DISEASE.  167 

a  few  instances,  when  the  process  is  softening,  and  it  has 
occurred  between  the  valves,  the  soft  matter  may  remain 
between  the  valves  some  time.  I  had  a  specimen — I  do 
not  know  but  I  may  have  it  now,  but  I  have  not  seen  it 
for  two  or  three  years — in  which  the  mitral  valve  was  the 
seat  of  atheromatous  deposit,  which  made  a  material 
looking  like  pus.  It  was  found  after  death.  It  at  first 
merely  separated  the  two  folds  of  the  mitral  valve,  and 
formed  a  kind  of  abscess.  The  quantity  of  softened  ma- 
terial it  contained  was  perhaps  half  a  teaspoonful ;  it  had 
not,  as  in  the  specimen  you  are  examining,  destroyed  the 
lining  membrane,  or  at  least  the  folds  of  the  valve. 

There  is  one  other  point  to  be  referred  to  in  this  con- 
nection. You  hear  a  good  deal,  or  something,  at  any 
rate,  of  bony  deposits  in  the  heart,  and  particularly  in  the 
valves.  They  almost  always  result  from  a  changed  athe- 
roma. The  atheromatous  matter  is  deposited  in  the 
valves,  and  there  is,  perhaps,  some  thickening,  too,  from 
inflammation,  produced  by  the  irritation  of  this  substance, 
and  at  length  absorption  of  the  material  takes  place  and 
calcareous  matter  is  deposited  instead.  I  shall  be  able  to 
show  you,  probably,  two  or  three  hearts,  perhaps,  some 
in  which  you  can  feel  the  bony  roughness  in  the  valves. 
Occasionally  this  bony  deposit  occurs  in  the  heart  itself. 

I  was  consulted  in  regard  to  a  physician  who  was  pretty 
well  advanced  in  life.  It  was  supposed  that  he  had  heart 
disease.  His  heart  was  beating  irregularly,  sometimes 
palpitating,  sometimes  beating  very  feebly,  and  he  was 
subject  to  fainting  spells.  On  examining  his  heart  I 
found  no  enlargement.  I  found  nothing  to  indicate  val- 
vular disease,  and  I  said,  from  the  manner  in  which  it  be- 
haved, there  must  be  some  disease  of  it,  but  I  cannot 
tell  what.  In  a  month  or  two  this  gentleman  died,  and  a 
post-mortem  examination  was  made,  and  a  mass  of  cal- 
careous matter  was  found  in  the  body  of  the  heart,  begin- 


l68  VALVULAR  DISEASE. 

ning  at  the  base,  and  extending  downward  an  inch  or 
more,  and,  to  a  certain  extent,  thickening  the  particular 
part  of  the  base  of  the  heart  in  which  it  was  deposited. 
It  had  crippled  the  heart  in  its  muscular  contractions,  and 
the  heart  resented  it  as  well  as  it  could,  but  it  could  not 
tell  the  story  to  the  outsider.  It  was  plain  that  the  heart 
was  not  working  properly,  but  why,  nobody  could  guess, 
because  there  are  other  forms  of  disease  that  behave  in 
the  same  way,  particularly  fatty  degeneration,  Quain's 
degeneration  of  the  heart.  You  can  frequently  see  that 
there  is  something  wTong  in  the  heart,  but  you  cannot 
tell  what  it  is.  This  atheromatous  matter  is  not  usually 
deposited  in  the  muscular  fibres  of  the  heart;  and  whether 
it  was  the  result  of  a  previous  deposit  of  this  material  in 
the  heart,  or  whether  it  was  a  bony  deposit  or  a  calcareous 
deposit  in  connection  with  atheroma,  I  cannot  tell.  The 
importance  of  atheroma,  then,  will  impress  itself  upon 
your  minds  mainly  with  reference  to  the  deposit  in  the 
valves  of  the  heart  and  the  formation  of  calcareous  or 
bony  concretions  in  the  valves,  or,  perhaps,  in  the  sub- 
stance of  the  organ.  There  is  no  way  of  distinguishing, 
before  death  these  several  forms  of  diseased  valves. 
You  cannot  tell,  as  you  hear  a  certain  murmur,  whether 
it  is  produced  by  inflammation  of  the  pericardium  or  by 
an  atheromatous  deposit,  or  atheromatous  deposits  that 
have  passed  into  calcareous  or  osseous  formation.  To 
determine  this  you  will  have  to  wait  until  after  death,  and 
as  almost  all,  and  probably  all,  the  vegetations  of  the 
valves  are  incurable,  to  distinguish  the  varieties  is  of  no 
practical  importance. 

A  remark  or  two  more  in  regard  to  endocarditis  before 
we  pass  to  diseases  of  the  valves  to  consider  them  in  de- 
tail. Endocarditis,  Hke  pericarditis,  is  very  apt  to  show 
itself  to  a  certain  degree  upon  the  heart  itself.  An  cede- 
matous  effusion  may  take  place  in  the  fibres  of  the  heart 


VALVULAR   DISEASE.  169 

exactly  as  you  see  an  oedematous  effusion  occurring  in 
the  leg  when  the  knee  is  the  seat  of  inflammation,  or  in 
the  arm  when  the  muscles  of  the  shoulder  are  involved 
in  inflammatory  disease,  as  rheumatism.  For  example, 
in  February  of  last  year  I  woke  one  morning  with  a  pain 
and  stiffness  in  the  left  shoulder.  I  found  that  I  could 
not  get  my  coat  on  without  assistance.  So  I  got  assist- 
ance to  put  on  my  coat  and  went  about  my  business. 
The  arm,  however,  grew  worse  and  worse,  and  I  recog- 
nized after  a  few  hours  that  I  had  rheumatism  in  the  del- 
toid muscle,  and  directly  my  arm  and  hand  began  to  swell 
and  my  hand  looked  very  fat.  As  soon  as  I  saw  it  swell- 
ing I  took  off  my  rings  for  fear  they  would  be  fastened 
upon  the  finger  and  could  not  be  gotten  off.  The  swell- 
ing continued  until,  after  a  pretty  free  use  of  the  bicar- 
bonate of  soda,  the  inflammation  was  subdued.  Then 
the  swelling  all  went  away.  So  in  the  heart,  the  parts 
neighboring  to  those  that  are  the  seat  of  inflammation 
may  become  the  seat  of  oedematous  effusion,  and  thus 
weaken  the  heart — the  same  thing  that  I  stated  to  you 
when  speaking  of  pericarditis.  Pericarditis  and  endocar- 
ditis commonly  occur  together,  and  of  course  there  will 
be  on  this  account  all  the  more  of  this  oedema  of  the 
heart. 

Dr.  Livingstone  does  not  believe  the  little  nodules  on 
the  edges  of  the  mitral  and  tricuspid  valves  are  of  in- 
flammatory origin,  for  out  of  136  autopsies  of  children 
either  stillborn  or  a  few  hours  old  up  to  three  and  a  half 
years  of  age,  he  had  never  failed  to  find  them  when  he  had 
looked  for  theiUy  and  he  says  they  are  the  more  pronounced 
the  younger  the  child.  He  does  not  admit  that  they  re- 
sult from  the  rupture  of  the  intravalvular  blood-vessels, 
causing  haematomata  from  which  the  blood  has  been  ab- 
sorbed and  only  a  semi-transparent  substance  remaining. 
But  he  is  inclined  to  the  idea  of  Richard  Pott,  that  they 


I/O  VALVULAR  DISEASE. 

are  the  remains  of  the  foetal  valve,  whatever  that  may  be. 
He  says :  "  They  are  composed  of  a  collection  of  the  normal 
elements  of  the  valve  and  do  not  appear  microscopically 
like  the  deposits  of  an  endocarditis." 

Dr.  Livingstone  raises  the  question  whether  the  nodules 
on  the  mitral  valve  or  the  movement  of  the  blood  through 
the  ductus  arteriosus  produced  the  systolic  murmur  heard 
at  the  apex,  or  whether  it  was  produced  at  foramen  ovale, 
citing  de  Gassicourt  as  authority  for  the  idea  that  the 
current  through  the  ductus  arteriosus  can  cause  a  mur- 
mur. 

Endocarditis  is  perhaps  the  most  prolific  cause  of  de- 
rangement of  the  valves,  and  it  may  occur  as  the  result 
of  acute  disease  commonly  associated  with  rheumatism, 
occasionally  found  in  connection  with  Bright's  disease, 
sometimes  occurring  in  the  course  of  measles,  and  rather 
frequently  in  the  dropsical  sequelae  of  scarlet  fever,  some- 
times occurring  in  septicaemia.  And  still  again,  I  told 
you  it  may  occur  independently  of  any  of  these  causes 
as  a  spontaneous,  I  might  say  almost  idiopathic  disease. 
That  it  does  occur  frequently  in  this  manner  is  rendered 
evident  by  the  large  number  of  persons  that  suffer  from 
disease  of  the  valves  who  have  not  had  any  sickness  pre- 
ceding the  development  of  heart  disease  ;  who.  have  not 
had  rheumatism  ;  who  do  not  remember  that  they  have 
had  scarlet  fever ;  who  have  not  had  Bright's  disease,  etc. 
I  have  told  you  of  atheroma,  a  particular  deposit,  more 
frequently  found  on  the  inner,  or  rather  under  the  inner, 
lining  of  the  arteries  encroaching  upon  the  elastic  tissues 
of  the  walls.  I  told  you  that  it  undergoes,  whether  in 
the  valves  or  in  the  artery,  one  of  two  changes  as  a  rule. 
It  may  soften  and  form  a  yellow  collection  looking  like 
an  abscess,  and  this  may  rupture  the  intima  and  escape 
into  the  blood,  and  do  mischief  or  not  according  to  the 
fineness  of  its  division.     Or  it  may  harden  and  undergo 


VALVULAR   DISEASE.  I7I 

calcareous  degeneration.  It  does  not  seem  possible  that 
the  elements  of  atheroma  can  be  converted  into  bony 
matter.  It  would  seem  altogether  likely,  therefore,  that 
it  is  substituted  for  these  after  they  are  softened  and  have 
been  absorbed.  I  told  you  that  this  deposit  in  the  valves 
causes  a  thickening,  an  inflammation,  a  bony  deposit 
especially  causing  constant  irritation.  I  told  you  that 
the  valves  are  sometimes  ruptured,  and  I  pointed  out  to 
you  a  specimen  in  which  the  inferior  or  lower  portion  had 
given  way,  so  as  to  render  that  part  of  the  valve  useless 
in  retaining  the  blood  in  the  artery.  I  told  you  of  a  case 
in  which  a  man,  while  lifting  a  heavy  beam,  felt  a  sudden 
something  give  way,  he  could  hardly  tell  what,  but  he 
said  there  was  something  gave  way,  and  he  fainted,  and 
sat  for  a  considerable  time  in  the  mill  before  he  attempted 
to  go  home,  and  then  reached  home  only  with  assistance. 
In  a  few  days  he  revived  again  and  went  to  his  work. 
He  lived  twelve  years  after  that  with  the  heart  largely 
hypertrophied.  At  the  post-mortem  the  longest  portion 
of  the  tricuspid  valve  was  found  to  have  been  flapping 
backward  and  forward  in  the  current  of  blood.  As  the 
blood  ran  down,  the  strand  was  in  the  ventricle,  and  when 
the  heart  contracted  it  would  double  back  on  the  rest  of 
the  valve.  A  tendinous  cord  had  given  way  when  he  had 
felt  the  sensation  described.  He  had  a  murmur  heard  in 
systole ;  not  in  diastole. 

The  valve  may  give  way  in  a  considerable  variety  of 
cases.  I  recall  one  of  a  gardener  who  had  loaded  his 
cart  too  heavily.  His  horse  could  not  draw  it,  and  he 
put  his  shoulder  to  the  rear  of  it  to  help  the  horse,  and 
exerting  about  all  his  strength,  he  also  felt  something 
give  way  and  was  very  much  crippled  after  that.  He 
came  to  Bellevue  Hospital.  There  I  had  an  opportunity 
of  examining  him  before  and  after  death.  A  portion  of 
one. of  the  folds  of  the  aortic  valve  had  given  way  in  his 


172  VALVULAR  DISEASE. 

case  and  I  thought  almost  without  previous  disease. 
Atheroma  is  a  very  common  precedent  of  the  breaking 
of  the  valves.  This  man  lived  about  two  years  after  the 
accident  occurred  to  him. 

I  once  was  with  a  gentleman  who  was  making  great 
haste  to  reach  the  top  of  a  hill.  He  was  within  about 
fifty  feet  of  it,  when  he  started  on  a  run  up  the  steep  ac- 
clivity. The  result  was  he  was  brought  into  the  same 
condition  as  the  gardener,  and  from  that  time  on,  as  long 
as  I  knew  him,  there  was  a  regurgitant  murmur  at  the 
aortic  opening.  He  broke  something  at  that  time.  Pre- 
cisely what,  whether  the  bottom  of  the  valve  gave  way, 
or  whether  it  split  down,  I  cannot  tell.  One  thing,  how- 
ever with  regard  to  the  splitting  of  a  valve  is  worthy  of 
notice.  You  remember  there  is  on  top  of  the  valve  a  kind 
of  cord,  and  immediately  below  that  cord  the  valve  is  not 
as  strong  as  at  the  edge.  The  common  way  for  a  valve 
to  break  is  to  give  way  at  the  cord,  and  it  vibrates  in  the 
current  of  blood,  and  frequently  makes  a  musical  sound, 
a  sort  of  ^olian  harp  sound ;  making  a  noise  that  is  not 
altogether  unlike  that  of  a  cord  stretched  across  a  little 
opening  in  a  window.  It  is  quite  a  musical  note,  and  I 
don't  know  that  there  are  any  other  circumstances  in 
which  that  musical  sound  is  produced.  Then  I  should 
add,  in  this  enumeration,  that  the  tendinous  cords  are 
occasionally  found  welded  together,  two  or  three  or 
more  of  them,  and,  of  course,  a  great  deal  crippled  in 
their  action.  In  certain  instances  the  two  folds  of  the 
mitral  valve  and  the  three  portions  of  the  aortic  valve 
grow  together,  in  the  latter  case  leaving  a  slit  by  which 
the  blood  can  go  out  and  by  which  it  will  return  in  re- 
gurgitation. How  in  the  world  that  can  occur  I  do  not 
know,  but  it  does  occur.  They  are  almost  always  thick- 
ened, so  that  they  do  not  play  freely  before  this  adhesion 
or  coalescence  takes  place.     But  moved,  as  they  are,  con- 


VALVULAR  DISEASE.  173 

tinuously,  by  the  current  and  reflux  of  blood,  it  is  very 
difficult  to  understand  how  these  three  portions  of  the 
aortic  valve  can  grow  together,  leaving  only  a  little  slit 
for  the  blood  to  pass  through.  It  is  easier  to  understand 
how  adhesion  may  take  place  between  the  two  curtains 
of  the  mitral  valve,  for  by  contraction  they  can  be  grown 
together,  and  contraction  is  affected  by  the  material  that 
is  deposited  between  the  two  folds  of  the  valve. 

I  will  put  in  your  hands,  now,  for  example,  a  few  speci- 
mens of  valvular  disease.  Here  is  one,  in  which,  as  you 
open  it  you  see  that  the  wall  is  the  seat  of  spots  of 
atheroma,  and  some  of  these  have  passed  into  a  calca- 
reous condition.  Even  the  valve  itself  is  shortened  and 
thickened,  but  not  remarkably.  In  this  one  the  aortic 
valve  is  very  much  diseased.  If  you  put  your  finger  on 
it  you  will  find  that  it  has  hard  scales  on  it.  It  is  not 
very  much  contracted,  except  one  fold  of  it.  One  fold  is 
thickened  and  hardened,  and  on  the  inside  of  it  is  a  little 
calcareous  matter.  This  has  been  a  pericarditis,  and  the 
outside  of  the  heart  is  roughened  by  the  adhesions  that 
formerly  existed  on  the  pericardium.  The  mitral  valve 
is  in  a  state  of  very  marked  stenosis,  that  is,  contracted, 
and  you  see  here  almost  nothing  of  the  tendinous  cords, 
they  are  shortened  so  much.  The  fleshy  columns  are 
a  little  elongated,  to  make  compensation  for  the  shorten- 
ing of  the  tendinous  cords.  This  is  a  striking  speci- 
men of  stenosis  of  the  mitral  valve,  and  in  this  con- 
nection it  may  be  that  we  shall  find  an  illustration  of  the 
rule  that  applies  to  such  cases  generally — that  is,  stenosis 
of  the  mitral  valve  induces  hypertrophy  of  the  right  ven- 
tricle ;  stenosis  of  the  left  auriculo-ventricular  valve  in- 
duces hypertrophy  of  the  right  ventricle,  and  frequently 
of  the  right  auricle,  and  also  sometimes  of  the  left  auricle. 
This  you  see  illustrated  here.  The  right  ventricle  is 
thicker  than  natural,  but  not  very  much  hypertrophied. 


174  VALVULAR  DISEASE. 

This  stenosis,  marked  as  it  is,  did  not  disturb  the  circula- 
tion as  it  sometimes  does.  Then  in  this  specimen  you 
have  two  lesions,  the  aortic  valves  thickened  and  a  little 
calcareous  deposit  in  them  ;  and  at  the  mitral  valves, 
stenosis. 

In  this  specimen  the  mitral  valve  is  thickened  and  hard, 
but  not  disorganized,  and  it  is  large  enough  to  allow  the 
circulation  to  go  on  with  ordinary  freedom.  The  aortic 
valves  are  thickened,  shortened,  and  hardened.  In  this 
specimen  the  aortic  valves  are  a  little  but  not  much  dis- 
eased. The  chief  lesion  is  probably  in  the  mitral.  You 
observe  the  mitral  valve  is  thickened,  not  exactly  disor- 
ganized. There  is  some  hypertrophy  of  the  heart.  This 
is  not  a  very  striking  specimen. 

Here  is  a  very  good  one,  and  opened  in  such  a  way 
that  you  can  see  the  change  that  has  taken  place;  it  is  in 
the  aortic  valves.  You  observe  they  are  contracted  in 
their  length,  contracted  in  height,  and  thickened,  but  not 
nearly  as  much  as  in  some  specimens  I  shall  show  you 
hereafter. 

Now  comes  the  question,  what  sort  of  disturbance  will 
these  lesions  of  the  valves  produce?  Of  course  it  will  be 
first  felt  in  the  circulation.  Let  us  take  a  mitral  stenosis, 
such  as  you  have  in  two  or  three  of  the  specimens  now 
going  round,  and  its  effects  are  perhaps  as  simple  as  the 
effects  of  any  of  these  lesions.  Indeed,  they  all  follow  in 
the  same  track  after  they  have  taken  the  first  step.  Re- 
member, now,  that  the  blood  in  the  left  auricle  has  just 
come  from  the  lungs,  and  it  is  seeking  its  way  into  the 
left  ventricle.  It  is  obstructed  at  the  valves  ;  well,  what 
will  that  do  ?  The  circulation  by  the  right  heart  we  are 
to  assume  is  natural.  The  blood  goes  into  the  general 
system,  and  empties  into  the  right  side  of  the  heart,  and 
from  that  is  thrown  into  the  lungs,  and  it  begins  to  come 
from  the  lungs  into  the  left  heart   and    is    obstructed 


VALVULAR  DISEASE.  175 

What  then  ?  The  first  thing  will  be  a  certain  amount  of 
engorgement  of  the  lungs.  They  receive  blood  faster 
than  they  can  discharge  it  ;  the  consequence  is,  therefore, 
an  engorgement  of  the  lungs,  greater  or  less,  depending 
upon  the  extent  of  the  stenosis.  Next  after  that  comes 
a  strain  upon  the  right  heart,  which  is  attempting  to  send 
blood  all  the  time  into  the  lungs,  and  associated  with 
this  may  be  what  is  called  an  emphasized  condition  of 
the  second  sound  in  the  pulmonary  artery.  That  is 
pretty  full  of  blood,  the  right  heart  pumps  more  into  it, 
the  reaction  is  stronger,  and  makes  the  valves  strike 
with  more  force  than  natural.  Hence,  there  may  be  an 
increase  in  the  second  sound  from  the  pulmonary  artery, 
in  an  instance  where  the  disease  is  at  all  considerable. 
Well,  what  more  ?  Stop  the  blood  from  coming  into  the 
right  heart  and  what  will  be  flooded  ?  Why,  every  impor- 
tant organ  of  the  body.  The  blood  cannot  return  from 
the  veins  with  anything  like  its  natural  freedom.  The 
liver  will  be  engorged,  the  spleen  will  be  engorged,  the 
brain  will  contain  more  blood  than  it  should,  the  face 
perhaps  will  be  a  little  puffy,  from  a  little  effusion  into 
the  tissues  from  the  veins.  The  veins  cannot  empty 
themselves  freely.  Little  clusters  of  enlarged  veins  are 
found  upon  the  surface  of  the  body,  chiefly  upon  the 
chest.  The  external  thoracic  veins  frequently  become 
enlarged.  There  is  general  hindrance  of  the  blood  in  the 
general  circulation,  because  there  is  obstruction  of  the 
blood  in  the  lungs,  and  consequently  obstruction  in  the 
right  heart,  to  which  the  blood  in  the  general  system 
should  naturally  go.  One  consequence  of  this  accident, 
then,  is  enlargement  of  the  liver  ;  not  in  all  cases,  not  in 
the  majority  of  cases,  but  now  and  then.  And  some- 
times quite  considerable  hypertrophy  of  the  heart,  and 
enlargement  of  the  spleen,  from  the  same  cause,  namely, 
obstructed  return  of  blood.     The  effect  upon  the  stomach 


176  VALVULAR  DISEASE. 

is   often   noticeable.      There   being   more   blood  in  the 
stomach   mucous   membrane,   the   digestive   membrane, 
than  can  be  used,  the  digestion  becomes  impaired.     It  is 
imperfect,  and  the  appetite  feels  the  effect  of  this.    Then, 
too,  the  effect  of  the  obstruction  is  sometimes  so  consid- 
erable as  to  hinder  the  contribution  of  the  thoracic  duct 
to  the  general  nutrition  of  the  body.     The  thoracic  duct, 
you  remember,  receives  the  material  that  is  digested  in 
the  intestine,  and  carries  it  to  a  vein   through   a   duct, 
and  that  vein  delivers  it  to  the  general  circulation.    Well, 
that  is  obstructed  also  ;  it  cannot  freely  give  its  nutritious 
fluid  to  the  blood,  and  it  not  infrequently  happens  that 
the   patient   becomes  pale,  in  consequence   of  imperfect 
nourishment,  though  he  may  eat  a  considerable  quantity 
of  food  ;  and  you  will  observe,  frequently — I  am  referring 
now  to  an  advanced  case — that  the  patient  speaks  of  his 
feet  "being  swelled,  particularly  at  night,  if  he   is  on  his 
feet  during  the  day,  and  you  observe  yourself  some  pufifi- 
ness    about    the    face.     You  will  particularly  be  able  to 
notice  what  has  been  called  the  tear  line  ;  that  is,  a  some- 
thing looking  like  a  silver  thread  or  a  thread  of  transpar- 
ent glass  lying  upon  the  upper  edge  of  the  lower  eyelid. 
It  is  a  little  oedema  of  the  conjunctival  covering,  and  as 
the  eyelid  presses  considerably  upon  the  eye  it  is  forced 
up  along  the  ridge,  above  the  tear  line.     There  may  not 
only  be  oedema  of  different  parts  of  the  body,  but  the 
whole  body  may  be  swollen.     The  kidneys  have  suffered 
congestion,  and  have  taken  on  a  condition  analogous  to 
that  of  Bright's  disease,  generally  the  large  white  kindey, 
and  they  are  unable  to  perform  their  function  properly. 
The  urea  remains  in  the  blood,  or  a  part  of  it,  at  any  rate, 
and  produces  its  systemic  effects.      The  urine  is  com- 
monly scanty,  sometimes  even  bloody,  and  there  is  not 
unfrequently  effusion  found  in  the  chest,  a  double  pleuritic 
effusion.      I  recently  examined  a   gentleman  from  the 


VALVULAR  DISEASE.  1 77 

country,  or  rather  from  a  distant  city,  who  had  been  ill 
for  some  months,  and  in  the  course  of  the  examination 
found  fluid  effusion  coming  nearly  up  to  the  lower  angle 
of  the  scapula  on  both  sides.  My  thought  was,  he  has 
Bright's  disease.  He  had  heart  disease,  for  his  heart  was 
enlarged,  but  there  was  no  valvular  murmur  at  the  time  I 
examined  him.  On  examining  the  water  I  found  it  con- 
tained a  large  quantity  of  albumen.  It  was  one  of  the 
cases  that  interested  the  late  Dr.  Stephens  so  much  when 
this  matter  was  first  investigated.  There  was  a  large 
amount  of  amorphous  urates  in  his  urine.  On  heating  it 
up  to  about  the  point  of  boiling,  it  became  cloudy  with 
albumen,  and  heating  it  till  it  boiled  it  became  almost 
thick.  I  have  a  scale  for  estimating  the  amount  of  albu- 
men in  the  urine,  ranging  from  one  to  ten.  Ten  repre- 
sents a  coagulation  of  albumen  in  the  tube,  so  that  noth- 
ing will  run  out  ;  invert  the  tube  and  nothing  is  dis- 
charged ;  the  whole  of  the  urine  is  imprisoned  in  the  co- 
agulated albumen.  When  there  is  but  a  trace  of  albu- 
men it  is  represented  by  one.  In  the  specimen  of  the 
patient  spoken  of  the  amount  of  albumen  was  represented 
as  six ;  or  more  than  half  of  the  urine  was  composed  of  al- 
bumen. I  did  not  know  that  this  gentlemen  had  Bright's 
disease  when  I  found  a  double  pleuritic  effusion  (although 
I  felt  pretty  sure  of  it),  for  double  pleuritic  effusion  does 
once  in  a  while  occur  with  Bright's  disease. 

This,  then,  is  substantially  the  series  of  consequences 
that  will  result  from  obstruction,  from  stenosis  of  the 
mitral  valve.  And  you  can  see  that  when  the  blood  is 
returned  through  this  valve,  that  is,  when  it  has  entered 
the  ventricle,  and  a  part  of  it  is  returned  into  the  auricle, 
that  it  is  going  to  do  exactly  the  same  thing  when  the 
condition  becomes  marked.  It  it  all  the  same,  save  that 
in  the  one  case  it  is  stenosis,  in  the  other  it  is  insuffi- 
ciency.    The  valve  is  incapable  of  serving  as  a  gate,  a 


178  VALVULAR  DISEASE. 

watch,  and  a  part  of  the  blood  that  enters  the  ventricle 
goes  back  into  the  left  auricle,  and  obstructs  the  blood 
that  comes  in  from  the  lung,  so  that  the  result  in  the  end 
is  exactly  the  same — congestion  of  these  various  parts, 
sometimes  cyanosis.  This  latter  belongs  also  to  mitral 
stenosis. 

Then  there  is  another  point  which  I  may  as  well  refer 
to  here.  You  sometimes  see  a  pulsation  in  the  veins  of 
the  neck,  the  jugular.  There  are  two  modes  in  which 
what  appears  a  little  like  a  pulsation  is  to  be  accounted 
for.  When  this  obstructed  circulation  occurs  the  vein  is 
seen  to  fill  in  expiration.  In  expiration  the  blood  does 
not  flow  so  freely  in  the  lungs  or  into  the  chest,  as  in  in- 
spiration, and  in  expiration  you  may  watch  the  vein  and 
see  it  fill,  but  it  fills  from  above.  It  is  not  a  wave  coming 
up  from  below.  About  the  only  conditions  in  which  the 
wave  will  come  up  from  below  are  when  there  is  insuf- 
ficiency of  the  tricuspid  valve,  that  is,  the  valve  of  the 
right  side  of  the  heart,  or  when  there  is  hypertrophy,  a 
tumor  like  an  aneurism  resting  upon  the  vena  cava  de- 
scendens.  In  either  of  these  cases  a  regular  wave  may 
come  up  the  vein,  but  I  know  of  no  other  condition  in 
which  it  does  occur ;  but  in  the  cases  referred  to  you 
observe  the  filling  of  the  vein  is  a  different  thing  from  an 
aneurismal  tumor.  It  is  not  necessary  to  dwell  longer 
upon  regurgitation  at  the  mitral  valve,  as  the  effects  of  it 
in  the  end  are  the  same  as  those  of  stenosis. 


VALVUI-AK  iJiSEASE.  179 


LECTURE   XII. 

VALVULAR   DISEASE — [Continued), 

Now  turn  to  the  aortic  valve,  to  the  two  conditions 
that  have  been  named — obstructive  disease  and  regurgita- 
tive,  or  direct  and  indirect,  jf  you  choose  to  so  call  it. 
When  there  is  obstruction  at  the  aortic  valve  the  sound 
produced  by  it  will  be  heard  in  the  contraction  of  the 
heart  in  systole,  and  it  will  be  loudest  at  the  base  of  the 
heart,  near  the  sternum.  This  may  exist  in  a  moderate 
degree  for  a  long  time,  and  no  very  grave  aonsequences 
result.  But  if  it  is  a  growing  disease,  if  it  is  a  form  of 
valvular  disease  that  is  irritating  in  itself,  like  a  spicula  of 
calcareous  matter  in  the  valve,  action  of  the  valve  will 
excite  an  inflammation,  and  cause  a  deposit  of  material 
that  can  contract  and  still  further  deform  the  valve. 
But  there  are  a  great  many  persons  who  can  carry  both 
mitral  regurgitation  and  aortic  obstruction  a  very  long 
term  of  years.  Indeed,  my  colleague,  the  late  Dr.  Gil- 
man,  came  to  me  with  mitral  disease  at  a  certain  time, 
and  he  said, ''  Am  I  going  to  die  of  it?"  ''  Well,  maybe," 
said  I,  "  but  I  think  you  will  live  twenty  years."  The 
years  rolled  on,  and  I  heard  nothing  more  of  it,  until 
at  length  Dr.  Oilman  came  to  my  house,  and  exclaimed : 
"  Doctor,  my  lease  is  out !  I  want  to  renew  it !"  He 
lived  about  four  years  after  this. 

I  remember  a  patient  who  carried  a  valvular  lesion  fifty 
years  before  a  fatal  sickness  occurred  ;  a  young  man,  at 
first,  all  activity,  but,  of  course,  he  could  not  go  up-hill  or 
up-stairs  as  well  as  other  people,  but  his  mind  was  active, 
and  as  an  evidence  of  his  industry,  in  the  old  time,  when 


l8o  VALVULAR  DISEASE. 

speculation  did  not  fill  a  man's  pocket  in  a  day,  he  had 
made  by  speculating  in  oil  a  million  of  dollars,  and  built 
up  the  fortunes  of  two  brothers  in  this  period  of  fifty 
years. 

I  am  in  the  habit,  in  this  connection,  of  referring  to  a 
certain  case  because  it  is  rather  impressive.  Many  years 
ago  I  had  occasion  to  listen  over  a  certain  gentleman's 
heart,  and  I  found  a  mitral  murmur.  He  appeared  per- 
fectly well,  and  I  went  on,  making  no  sign  of  surprise, 
and  afterwards  thought  the  'thing  over.  He  is  of  phleg- 
matic temperament,  and  I  do  not  think  he  will  be  very 
much  excited  ;  he  will  take  the  world  pretty  easy  ;  I 
think  he  will  take  the  world  quite  as  easy  without  as  with 
a  knowledge  of  the  disease  of  his  heart.  Now  that  gen- 
tleman is  in  active  practice  to-day  ;  you  see  his  name  not 
infrequently  in  the  medical  journals,  as  having  performed 
this  or  that  operation,  and  he  is  a  great  deal  happier  than 
he  would  be  if  he  knew  that  he  had  mitral  regurgitation. 
There  is  no  knowing,  then,  when  the  unfavorable  issue 
will  take  place  ;  but  I  can  tell  you  this  about  it :  when  a 
patient  comes  to  you  complaining  of  a  great  deal  of  short- 
ness of  breath,  when  he  has  oedema  of  the  feet,  and  pos- 
sibly some  swelling  of  the  face,  look  to  the  kidneys. 
They  probably  have  become  involved  by  that  time,  and 
in  a  few  weeks,  in  a  Aveek  or  two,  he  may  be  pretty 
gravely  sick,  having  carried  disease  of  the  heart  for 
twenty,  thirty,  forty,  or  possibly,  fifty  years,  as  in  the 
case  I  have  just  referred  to.  And  here  it  is  perhaps  proper 
to  say  that  the  last  generation  of  doctors,  and  the  present 
generation  of  people  who  are  not  doctors,  look  upon  the 
statement  that  they  have  heart  disease  as  equivalent  to 
signing  their  death  warrant.  The  profession  have  out- 
grown the  idea  that  heart  disease  must  be  fatal  in  a  few 
months ;  but  the  older  physicians,  physicians  of  past  gen- 
erations, not  having  auscultation  to  guide  them,  were  not 


VALVULAR   DISEASE.  l8l 

able  to  detect  diseases  of  the  heart  until  the  kidneys,  and 
perhaps  liver,  and  possibly  the  spleen  were  involved.  In 
other  words,  not  until  oedema  came.  Their  post-mortem 
examinations  told  them  what  oedema  meant.  They  were 
able  to  recognize  then,  by  the  general  signs,  what  was 
the  trouble,  but  the  patients  generally  died  pretty  soon, 
in  a  few  months  after  the  oedema  occurred.  But  they 
may  have  passed  forty,  fifty,  or  even  sixty  years  before 
that,  with  the  same  disease  of  the  heart,  only  it  had  not 
until  the  oedema  appeared,  come  to  be  obstructive  to  the 
venous  circulation. 

But  to  go  on  with  the  obstruction  at  the  aortic  opening. 
If  it  is  moderate  there  is  compensation.  The  heart  has 
the  faculty  of  growing  in  size  and  in  strength  to  meet  an 
emergency,  and  we  speak  of  compensating  hypertrophy 
of  the  heart.  If  the  blood  does  not  flow  easily  through 
the  aortic  opening,  the  heart  will  gain  additional  strength 
by  gaining  additional  fibres,  and  will  overcome  the  obsta- 
cle, so  that  a  man  may  carry  a  disease  of  that  kind  a  great 
while  without  knowing  that  he  has  it.  But  when  regur- 
gitation occurs,  and  that  is  only  in  the  advanced  stages  of 
obstructive  disease,  when  the  valves  become  shortened 
and  thickened,  so  that  they  cannot  fall  together,  a  certain 
quantity  of  blood  that  has  been  sent  into  the  aorta  goes 
back  again  into  the  ventricle  every  time  the  heart  dilates, 
and  here  is  work  to  be  done  over  and  over  again.  The 
heart  has  to  do  its  work  twice  over,  substantially ;  at  any 
rate,  once  and  a  half.  The  ventricle  has  just  been  filled 
from  blood  forced  in  from  the  auricle,  and  half  filled  from 
that  which  comes  from  the  aorta.  The  effect  of  this  is  ex- 
actly that  which  I  have  been  describing  to  you,  and  you 
will  see  how  it  must  be  so.  When  blood  from  the  aorta 
falls  back  into  the  left  ventricle  it  prevents  blood  from 
coming  in  from  the  left  auricle.  Only  about  half  the  con- 
tents of  the  ventricles  can  come  in  from  the  left  auricle, 


1 82  VALVULAR   DISEASE. 

and  consequently  the  blood  will  set  back  upon  the  right 
heart,  and  engorge  the  lungs,  and  it  will  also  produce  very 
much  the  same  general  symptoms  as  those  I  have  de- 
scribed to  you.  Well,  then,  these  all  come  to  about  the 
same  thing.  Their  consequences  are  substantially  the 
same.  So  also  in  contraction  of  the  mitral  valve.  A 
contraction  of  the  aortic  valve,  you  observe,  is  compen- 
sated for  very  generally,  and  that  is  not  so  grave  a  trouble. 
A  stronger  current  of  blood  is  sent  over  it,  and  of  course 
into  the  general  circulation  more  blood  is  sent  in  a  given 
time,  and  consequently  the  general  circulation  does  not 
feel  it  so  much.  These  are  the  general  effects  relating  to 
the  advanced  stage  of  cardiac  disease. 

The  question  has  been  often  raised  and  discussed,  which 
comes  first,  the  kidney  disease  or  the  cardiac  disease? 
My  own  answer  is  very  positive :  that  while  the  cardiac 
disease  may  come  after  the  kidney  affection  has  begun, 
in  the  great  majority  of  instances  in  which  they  are  con- 
nected, the  connection  is  as  I  have  been  describing  to 
you.  The  kidneys  become  congested  because  the  circu- 
lation is  obstructed  at  the  heart,  and  after  they  have 
suffered  a  certain  length  of  time  they  will  begin  to  give 
albuminous  urine ;  they  do  not  secrete  the  urea  in  full 
measure,  and  cede*ma  then  begins  in  different  parts  of  the 
body.  It  is  my  strong  conviction  that  in  nine  cases  out 
of  ten  where  the  two  are  associated  the  cardiac  disease 
came  first,  and  the  other  case  will  be  an  instance  in  which 
kidney  disease  from  some  other  cause  has  occurred,  and 
the  cardiac  disease  has  followed  ,it,  possibly  by  the  influ- 
ence of  congestion  in  a  certain  degree.  But  the  order  is 
almost  always  cardiac  disease  first,  and  renal  disease 
afterward.  I  have  noticed  so  often  what  I  have  already 
explained  to  you  that  I  cannot  have  a  doubt  about  it.  I 
examine  a  man  and  find  he  has  valvular  lesion  of  one  sort 
or  another ;  I  watch  him  for  a  year ;  he  gets  along  very 


VALVULAR  DISEASE.  1 83 

well ;  and  perhaps  ten,  fifteen,  or  twenty  years  after  I 
have  examined  him  for  the  first  time  he  begins  to  suffer ; 
he  begins  to  get  oedema  of  the  lungs,  which  is  one  of  the 
effects  I  have  not  mentioned.  We  may  have  an  oedema- 
tous  condition  of  the  lungs,  as  well  as  of  the  legs,  body, 
and  face. 

With  reference  to  the  right  side  of  the  heart,  we  have 
had  but  little  experience  with  disease  of  the  valves  on  this 
side.  For  forty-nine  cases  of  valvular  disease  of  the  left 
heart  there  will  hardly  be  one  of  valvular  disease  of  the 
right  heart.  I  have  told  you  that  after  birth  the  left  side 
of  the  heart  is  the  seat  of  disease,  and  before  birth  the 
right.  In  the  right  heart  there  are  lesions  of  the  valves, 
though  they  are  rarely  met  with.  In  a  little  boy  about 
e-ight  years  old,  when  the  college  was  in  Crosby  Street,  I 
found  a  very  peculiar  sound  in  listening  over  the  base  of 
the  heart.  It  was  not  a  murmur,  but  it  was  a  snap,  and 
it  was  heard  in  both  actions  of  the  heart.  It  was  a  double 
snap,  very  much  such  as  you  get  by  pulling  a  piece  of 
ribbon  suddenly.  He  died,  and  at  the  post-mortem 
examination  that  sealing  together  of  the  pulmonary  valves 
was  found  which  I  have  already  described  to  you.  The 
edges  of  the  three  portions  of  the  valve  were  sealed 
together,  with  the  exception  of  an  openings  which  must 
have  been  less  than  half  an  inch  in  the  middle,  and  one 
of  the  lips  of  that  opening  was  a  little  longer  than  the 
other,  and  it  was  this  which  snapped  when  the  blood 
came  against  it  from  the  heart,  and  snapped  again  when 
the  pressure  from  the  artery  was  felt.  That  was  the  only 
lesion  about  it.  I  did  not  distinguish  that  from  the  aortic 
disease,  for  it  is  a  difficult  thing  to  do  it,  but  some  per- 
sons claim  to  be  able  to  do  so  by  getting  the  sounds  of 
he  pulmonary  valves  a  little  to  the  left  of  the  sounds 
that^come  from  the  aorta.  I  dare  not  trust  my  ear  for 
the  diagnosis ;  and  besides,  there  is  another  mode  that  is 


1 84  VALVULAR  DISEASE. 

worth  something,  but  not  worth  a  great  deal  either,  and 
that  is,  if  the  sound  is  at  the  base  of  the  heart,  to  follow 
it  to  the  artery,  and  particularly  to  the  left  and  right 
clavicle.  Listen  to  the  sound  from  the  heart  there ;  if  it 
comes  up  there  pretty  fully,  it  is  in  all  probability  in  the 
aorta.  I  say,  in  all  probability.  I  make  that  modifica- 
tion because  the  two  vessels,  the  pulmonary  artery  and 
the  aorta,  are  sealed  together  by  loose  connective  tissue, 
and  for  a  certain  distance  after  they  leave  the  heart  they 
run  together. 

I  have  some  curiosities  here,  some  that  are  so  rare  that 
you  may  never  see  anything  like  them,  and  some  that  you 
will  see  plenty  of.  Here,  for  example,  is  a  heart,  the  peri- 
cardium of  which  is  attached  to  the  heart,  but  between 
the  pericardium  and  the  heart  is  a  layer  of  bone  that 
makes  a  perfect  hoop,  or  did  make  a  perfect  hoop  about 
the  heart.  This  bony  material,  you  observe,  is  covered 
over  by  the  pericardium  on  the  outside,  and  attached  to 
the  heart  on  the  inside.  It  flattens  out  to  make  quite  a 
broad  covering,  then  it  grows  narrow,  and  is  broken,  and 
you  can  feel  the  rough  bone  on  each  side — it  then  goes 
on  up  to  the  point  of  starting.  How  a  heart  hooped  in 
this  way  could  pump  out  blood  is  a  matter  of  wonder. 
It  was  probably  by  a  change  in  its  usual  motion.  The 
contraction  was  probably  from  the  point  towards  the  base. 
There  is  also  in  this  heart  a  considerable  amount  of 
thickening  and  hardening  of  the  aortic  valves,  but  not 
so  much  as  in  some  specimens  I  shall  show  you.  The 
amount  of  effusion  that  took  place  during  the  pericarditis, 
between  the  pericardium  and  the  heart,  was  too  large  to 
undergo  organization,  and  for  some  reason  bony  matter 
has  taken  its  place.  It  was  very  likely  broken  down  and 
absorbed  in  part,  and  calcareous  matter  deposited  in  its 
place. 


VALVULAR   DISEASE.  1 85 

Here  is  a  heart  that  I  shall  have  occasion  to  refer  to, 
perhaps,  at  our  next  meeting.  Observe,  particularly,  its 
flabbiness,  and  its  color,  which  is  yellow.  This  color  is 
not  so  very  deeply  marked,  however.  It  is  a  fatty  heart. 
It  is  an  example  of  Quain's  degeneration.  It  is  a  feeble 
heart  also ;  the  walls  are  hardly  of  the  usual  thickness. 
But  I  will  touch  on  this  again  further  on.  I  have  but 
little  more  to  say  regarding  valvular  diseases.  I  told  you 
that  the  valves  are  occasionally  torn  out ;  the  aortic 
valves  are  torn  out  at  the  bottom,  at  the  attachment  to 
the  aorta.  The  cup  is  made  no  cup  by  having  its  bottom 
fall  out,  so  to  speak.  That  is  almost  always  the  conse- 
quence of  atheromatous  degeneration,  weakening  the 
valve  at  that  point.  There  is  another  atheromatous 
change  that  is  met  with  occasionally,  and  that  is  athero- 
matous deposit  at  the  point  where  two  of  these  valves 
are  together  attached  to  the  aorta.  You  will  observe  as 
you  examine  these  specimens  that  each  pair  of  the  valves, 
each  of  the  two  valves  that  are  near  to  each  other,  have 
their  attachment  to  the  aorta  at  the  same  position ;  that 
is,  one  is  in  immediate  apposition  to  the  other.  Now,  it 
sometimes  happens  that  the  aorta  at  that  point  becomes 
atheromatous,  and  that  the  attachment  is  torn  down.  It 
is  torn  down  so  that  it  comes  to  be  about  a  quarter  of  an 
inch  below  the  attachment  of  the  other  valve,  and  this 
produces  insufificiency.  The  valves  will  not,  even  suppos- 
ing they  are  not  diseased,  meet  in  the  middle  of  the  aorta ; 
one  will  fall  in  below  the  others,  and  consequently  the 
valve  is  incomplete. 

These,  I  think,  with  those  enumerated  before,  will  con- 
stitute the  changes  which  you  will  be  most  likely  to  meet. 
Possibly  not  all  the  changes,  but  they  are  all  that  occur 
to  me  as  occurring  with  any  degree  of  frequency. 

There  is  a  point  which  I  omitted  to  refer  to,  but  was 
reminded  of  by  one  of  the  students,  and  that  is  with  re- 


1 86  VALVULAR  DISEASE. 

gard  to  the  pulse  in  regurgitation  at  the  aortic  opening. 
There  is  a  peculiar  pulse.  It  has  not,  as  our  Methodist 
friends  say,  the  gift  of  continuance.  It  is  a  blow,  short, 
sharp,  I  cannot  say  decisive,  and  then  it  seems  as  if  the 
pulse  is  instantly  cut  off  as  soon  as  you  feel  it.  There  is 
a  little  duration  to  the  swelling  of  the  artery  in  the  healthy 
condition,  and  still  more  in  hypertrophy  of  the  heart. 
Supposing  there  is  no  obstacle,  but  if  there  is  regurgita- 
tion at  the  same  time,  the  pulse  has  that  short,  quick,  sud- 
den beat  aud  sudden  subsidence;  the  force  that  created  the 
pulse  seems  to  be  withdrawn  instantly  after  you  feel  the 
pulse,  and  then  there  is  not  infrequently,  on  account  of 
the  smaller  wave  of  blood  that  is  sent  out,  a  little  retarda- 
tion ;  that  is,  the  pulse  does  not  come  to  the  finger  as 
soon  after  the  heart-beat  as  in  health.  But  this  you  can 
only  appreciate  by  putting  one  hand  on  the  praecordial 
region  and  the  other  on  the  pulse.  The  arteries  in  the 
neck,  in  instances  of  hypertrophy  and  regurgitation  at  the 
aortic  opening,  are  apt  to  be  enlarged  and  to  have  a  wide 
beat.  You  observe  I  do  not  say  stronger  beat,  but  a 
wider  beat  than  usual,  and  the  pulse  in  them  is  apt  to  be 
feeble ;  and  further,  the  arteries  in  time  not  infrequently 
grow  tortuous — they  wind  about  instead  of  going  direct  to 
the  point  of  distribution. 

From  a  number  of  examinations  of  hypertrophied 
hearts,  with  valvular  lesions,  Dr.  Putjatin*  concludes  that 
in  chronic  affection  the  nerve  ganglia  are  affected  by  an 
inflammatory  process.  In  early  and  slight  disease  the 
changes  are  limited  to  hyperaemia  and  granular  de- 
generation. In  chronic  and  extended  disease  of  the  heart 
the  connective  tissue  is  produced  and  there  is  fatty  and 
pigment  degeneration  of  ganglion  cells.  In  one  case  there 
was  entire  destruction  of  the  ganglion  cells  and  calcifica- 

*  The  Medical  Record,  July  7,  1883. 


VALVULAR   DISEASE.  18/ 

tion  of  the  tissues  between  them.  Changes  in  the  ganglia 
may  also  be  produced  by  chronic  constitutional  disease. 
In  this  fact  may  be  found  the  explanation  of  the  function 
disturbances  and  even  paralysis  of  the  heart. 

Another  observer  found  that  in  hypertrophy  with  chro- 
nic interstitial  nephritis  with  the  growth  of  the  muscular 
tissue  the  medullary  sheath  of  the  nerves  is  lost,  and  a 
process  of  nuclear  proliferation  commences.  Should  an 
acute  disease  supervene,  then  the  change  in  the  affected 
nerves  assumes  the  character  of  an  acute  parenchymatous 
inflammation.  In  the  nerve  cells  lying  in  the  course  of 
the  fibres  as  well  as  those  in  the  ganglia  of  the  septum 
arteriosus  the  changes  were  confined  to  thickening  of  the 
capsule  and  increase  of  the  nuclei.  The  protoplasm 
itself  was  not  affected. 

As  bearing  upon  valvular  disease  of  the  heart  both  in 
reference  to  etiology,  pathology,  diagnosis,  and  treatment, 
I  have  collected  several  cases,  some  from  those  which 
have  come  under  my  own  observation  and  others  which 
have  been  reported  in  current  medical  literature,  and  shall 
also  enumerate  various  experiments  which  have  been 
made,  and  conditions  which  have  been  observed  in  valvu- 
lar diseases  of  the  heart. 

Dr.  C.  S-  M.,  seventy  years  of  age,  applied  to  me  forty 
years  ago  for  advice  regarding  a  disorderly  heart.  I  found 
that  he  had  moderate  enlargement  and  a  murmur,  I  think 
mitral  chiefly,  because  he  has  now  that  murmur  feebly, 
and  no  murmur  at  the  aortic  opening.  He  was  advised 
to  eat  moderately,  not  to  walk  up  hill  when  he  could  ride, 
and  when  obliged  to  do  this  to  take  plenty  of  time,  and 
go  very  slowly ;  as  his  profession  would  compel  him  to 
ascend  stairs  many  times  a  day,  to  apply  the  rule  of  mod- 
eration with  great  rigor  to  this  part  of  his  duty.  He  has 
lived  in  obedience  of  these  rules.  He  has  taken  no  intox- 
icating liquors  except  when  needed  as  medicine.      He 


1 88  VALVULAR  DISEASE. 

has  had  nearly  all  his  professional  life  a  large  practice, 
but  as  soon  as  he  had  won  the  confidence  of  his  patients 
sufficiently  to  do  so  he  refused  to  go  out  after  bedtime, 
and  has  long  had  a  partner  on  whom  that  work  has  de- 
volved. He  has,  until  lately,  appeared  like  a  healthy 
man,  and  it  is  only  in  the  last  four  months  that  he  has 
not  been  able  to  follow  his  practice.  A  month  and  a  half 
ago  he  came  to  my  house  suffering  from  shortness  of 
breath,  and  having  some  cedema  of  the  legs,  and  fluid  in 
each  pleural  cavity,  filling  one  half  its  capacity.  He 
took  diuretics.  The  kidney  secretion  soon  amounted  to 
seventy  ounces  a  day,  and  he  improved  rapidly,  so  that 
he  felt  that  he  was  all  but  restored  to  health,  and  ceased 
to  take  any  medicine.  He  went  from  home,  as  he  says, 
"  on  a  summer  vacation."  While  away  the  urine  dimin- 
ished in  quantity  to  three  or  four  ounces,  was  of  very 
high  color,  and  highly  albuminous.  With  this  came  con- 
vulsions, and  he  had  of  these  in  a  day  and  a  half  they  say 
thirty,  none  very  violent,  but  all  with  a  short  period  of 
unconsciousness.  With  a  digitalis  poultice  over  the  loins 
and  other  medicines  the  urinary  secretion  was  restored  to 
a  healthy  quantity  and  more,  and  he  has  had  no  more 
convulsions.  After  recovering  some  strength  he  returned 
to  his  home,  where  I  saw  him  to-day  (Aug.  23,  1883). 

He  has  now  no  oedema  at  all.  The  fluid  is  wholly  re- 
moved from  the  chest,  but  he  has  lost  flesh  since  I  saw 
him  a  month  and  a  half  ago,  yet  for  most  of  the  time  he 
has  taken  about  his  usual  rations,  avoiding  meat  since 
the  convulsions,  but  taking  milk  and  eggs.  The  urine 
amounts  to  thirty  ounces  and  over  daily,  and  he  says  he 
feels  well  but  is  not  strong.  He  walks  the  floor,  but  is 
not  willing  to  go  down  stairs,  fearing  he  cannot  get  back 
Albumen  had  not  been  found  when  I  saw  him  first,  and 
no  casts;  but  I  felt  certain  of  Bright's  disease  because 
it  so  often  follows  heart  disease  even  forty  years  after  the 


VALVULAR  DISEASE.  1 89 

discovery  of  the  heart  affection  ;  and  because  there  was 
double  pleural  serous  effusion,  without  pain,  or  other 
evidences  of  pleurisy,  and  because  with  these  there  was 
oedema  of  the  legs.  I  did  not  examine  the  urine,  but 
others  have ;  and  since  his  first  call  on  me  albumen  has 
been  found,  uniformly,  more  or  less  varying,  and  casts 
not  uniformly,  but  often,  mostly  hyaline. 

Now  comes  the  peculiarity,  to  record  which  I  have 
written  up  the  case.  When  I  saw  the  doctor  in  July  I 
made  out  a  double  mitral  murmur,  which  was  not  very 
distinct  to-day,  but  his  pulse  at  the  wrist  was  twenty-eight 
beats  in  the  minute^  and  no  faint  indication  even  of  any 
more.  But  when  the  impulses  of  the  heart  were  counted 
by  putting  the  ear  over  it,  there  were  twenty-eight  pul- 
sations that  were  distinct  and  strong,  and  twenty-eight 
more  alternate  ones  which  could  just  be  heard  and  no 
more,  and  which  sent  no  pulse  to  the  wrist.  Occasionally 
the  feeble  heart  pulse  would  be  strong  and  forcible,  but 
for  almost  the  whole  of  a  minute  it  was  the  faint  and  the 
strong  alternately. 

Dr.  Herman  Tittenger*  describes  a  peculiar  murmur 
characterized  by  the  distance  at  w'hich  it  is  audible  (it 
can  be  distinctly  heard  through  the  bed  covering)  by  its 
stability  (it  is  but  slightly  influenced  by  the  intensity  of 
the  heart's  action)  and  by  its  character.  Together  with 
the  murmur  is  perceived  a  widely  propagated  tremor. 
This  phenomenon  occurs  only  with  rupture  of  the  valves 
or  tendinous  cords.  The  primary  murmur  is  caused  by 
insufficiency  of  the  valves,  the  secondary  sound  by  the 
flapping  of  the  loose  valves  and  tendinous  cords  in  the 
returning  blood  stream.  A  diastolic  murmur  indicates 
the  rupture   of  the  semi-lurrar  valves,   while    a   systolic 

*  Medical  Record,  Aug.  18, 1883,  p.  184,  from  Centralb.Jiir  Klin.  Med., 
June  9,  1883. 


190  VALVULAR  DISEASE. 

sound  points  to  the  (much  less  frequent)  lesion  of  the 

mitral  valve. 

Aneurismal  Dilatation  of  the  Heart  and  Mitral  Steno- 
sis— Fibroid  Induration!^ — The  heart  is  large ;  the  ante- 
rior wall  of  the  left  ventricle  is  bound  to  the  pericardium 
by  a  firm  band  of  connective  tissue.  The  left  ventricle  is 
enormously  dilated,  and  the  left  ventricular  wall  in  places 
is  less  than  one  eighth  of  an  inch  in  thickness,  and  at  the 
apex  there  is  a  portion  of  the  wall  where  the  pericardium 
and  endocardium  are  separated  only  by  the  interposition 
of  a  thin  layer  of  fat.  Posteriorly  the  ventricular  wall 
is  much  thicker,  being  uniformly  nearly  one  inch.  The 
papillary  muscles  are  much  hypertrophied.  The  right 
ventricle  is  moderately  dilated,  and  the  valves  of  that  side 
are  normal.  The  segments  of  the  aortic  valve  are  slightly 
thickened  and  retracted.  The  stenosis  of  the  mitral  valve 
only  admits  a  cylinder  of  half  an  inch  diameter.  The 
endocardium  is  markedly  thickened,  and  in  all  the  ven- 
tricular wall  there  is  increase  of  the  fibrous  tissue  be- 
tween the  muscular  cells  (fibroid  induration  of  the  heart) 
especially  marked  where  the  ventricular  wall  is  thinnest, 
except  at  the  apex,  where  there  is  no  muscular  tissue. 
There  is  atrophy  of  the  fibre  cells,  and  much  pigment 
arranged  around  the  poles  of  their  nuclei.  The  cells  in 
places  contain  a  small  amount  of  fat,  but  generally  the 
transverse  striae  are  well  preserved. 

Dr.  Ferguson,  who  reported  this  case  to  the  N.  Y. 
Pathological  Society,  May  23,  1883,  has  examined  the 
most  of  it.  He  finds  parts  hypertrophied,  parts  dilated, 
in  parts  fibroid  substitution  for  muscular  fibres,  and  here 
and  there  a  little  fatty  degeneration  of  the  muscular 
fibres.  The  patient  was  twenty-seven  years  of  age ;  had 
had  rheumatism.     His  chief  suffering  was  from  dyspnoea 


*  Med.  Rec,  Sept.  8,  1883. 


VALVULAR   DISEASE.  I9I 

and  palpitation,  cough  and  expectoration,  the  latter 
scanty  and  sometimes  streaked  with  blood.  There  was 
a  double  mitral  murmur.  Pulse  80  to  140,  temp.  99°  to 
102°.  He  died  unexpectedly.  A  complete  diagnosis  was 
impossible. 

Dr.  Ferguson  exhibited  at  the  meeting,  June  27,  1883, 
a  heart  resembling  this  with  aneurismal  clots  adherent 
near  the  apex  in  the  left  ventricle,  wall  there  thin  and 
wholly  fibrous,  muscular  tissue  gone. 

Tricuspid  Insufficiency. — M.  Frangois  Franck,*  by  a 
specially  contrived  valvulotome,  has  produced  tricuspid 
insufficiency  and  has  noted  the  effects,  i.  Systolic  pul- 
sation in  the  jugular  veins  and  in  the  thoracic  veins,  dila- 
tation and  hepatic  pulsation.  2.  Systolic  murmur  in  the 
heart,  whose  pitch  is  in  inverse  proportion  to  the  extent 
of  the  sound ;  increased  frequency  of  cardiac  action ; 
diminution  in  the  arterial  pressure.  3.  Increased  fre- 
quency of  respiration  ;  and  4.  After  a  time  the  phenomena 
of  general  venous  stasis  ? — ascites,  anasarca,  albuminuria, 
etc. 

M.  P.  Dureoziez  concludes  that  a  tricuspid  regurgitant 
murmur  can  be  heard  over  the  entire  anterior  surface  of 
the  heart,  the  points  of  maximum  intensity  being  some- 
times at  the  xiphoid  cartilage,  sometimes  at  the  cardiac 
apex,  and  it  may  be  heard  at  the  latter  spot  only.  It  is 
not,  however,  transmitted  to  the  axilla ;  and  is  not  heard 
in  the  back.  It  is  not,  necessarily,  associated  with  venous 
pulsation. 

Mitral  Obstruction  and  its  Consequences. — Dr.  E.  R. 
Bruch,f  at  a  meeting  of  the  Pathological  Society  of  Phil- 
adelphia, exhibited  a  heart  the  mitral  opening  of  which 
was  nearly  occluded  by  an  epigglotic-shaped  enlargement 


*  N.   Y.  Med.  your.,  March  3,  1883. 
\  Ibid. 


ig2  VALVULAR  DISEASE. 

of  one  of  its  leaflets,  permitting  during  life  reflux.  The 
result  was  dilatation  and  hypertrophy  of  the  left  auricle 
to  twice  its  proper  size.  The  right  ventricle  is  very  much 
dilated,  the  walls  of  less  than  half  their  proper  thickness, 
and  the  capacity  of  its  cavity  doubled.  The  tricuspid 
valve  was  insufficient  on  accourtt  of  this  dilatation.  There 
was  during  life  a  broad  area  of  dulness,  extending  to  the 
right  of  the  median  line.  The  murmur  heard  was  both 
systolic  and  presystolic.  The  second  sound  was  much 
accentuated.  The  first  sound  was  distinct  over  the  ven- 
tricle, but  obscured  by  the  murmur  at  the  apex.  The 
immediate  cause  of  death  was  pulmonary  repletion  with 
blood  which  induced  right  heart  failure,  as  in  cases  of 
aortic  obstruction  it  is  induced  by  left  ventricle  failure. 

Pleurisy  with  Heart  Disease. — Dr.  Bucquoy*  has  ob- 
served a  number  of  cases  of  pleurisy  occurring  in  the 
course  of  heart  disease.  He  says  that  though  the  patient 
may  be  weak  from  this  disease  of  the  heart  often  associ- 
ated with  albuminuria,  the  inflammation  has  all  the  char- 
acteristics of  subacute  idiopathic  pleurisy,  and  is  entirely 
distinct  from  hydrothorax.  It  usually  pursues  a  favora- 
ble course,  ending  at  length  in  absorption.  He  would 
hasten  a  cure,  and  if  absorption  is  tardy  recommends  tap- 
ping, especially  if  there  is  dyspnoea  or  other  urgent  car- 
diac symptom's. 

Mitral  Stenosis — Prognosis. — Dr.  Dureoziez  f  finds  that 
mitral  stenosis,  simple  or  combined  with  other  valvular 
diseases,  permits,  in  exceptional  cases,  the  life  to  pass  the 
sixtieth  year.  The  complication  of  mitral  regurgitation 
does  not  aggravate  the  prognosis.  The  co-existence  of 
aortic  insufficiency  renders  it  more  grave.  The  complica- 
tion of  tricuspid  lesion  is  of  very  serious  import. 


*  The  Med.  Rec,  March  lo,  1883. 
f  Ibid,  Oct.  27,  1883. 


VALVULAR  DISEASE.  I93 

Aortic  Regurgitation  Make$  the  Pulmonary  Second 
Sound  Inaudible. — Every  auscultator  has  noticed  that  the 
sound  of  aortic  regurgitation  may  be  pretty  loud  at  the 
base  of  the  heart,  and  at  the  same  time  be  nearly  or  quite 
inaudible  at  the  apex.  This  is  not  true  of  the  louder 
class  of  murmurs,  but  is  true  of  those  which  are  loud 
enough  to  obscure  or  wholly  cover  the  pulmonary  second 
sound.  It  is  possible,  in  such  case,  to  find  the  pulmon- 
ary second  sound  audible,  more  or  less  clearly,  at  the 
apex,  while  the  regurgitant  sound  will  be  conducted 
down  the  sternal  bone  much  more  loudly  than  down  the 
heart  tissues.  Dr.  Begbie  has  called  attention  to  these 
facts. 

Stenosis  of  the  Right  Auriculo-Ventricular  Opening. — 
Dr.  Kucher  reports  the  cure  of  a  child  twenty-four  hours 
old  in  whom  the  right  auricle  was  larger  than  the  left,  the 
borders  of  the  thin  curtains  of  the  tricuspid  valve  were 
sealed  together,  and  made  a  funnel  with  two  openings  in 
the  bottom  of  the  funnel  that  would  admit  a  Simpson*s 
sound.  The  material  of  the  valve  was  thickened  and 
hard.  This  he  ascribes  to  fcetal  endocarditis  confined  to 
this  valve. 

He  also  found  in  the  left  auriculo-ventricular  opening 
a  transverse  chorda  tendinea,  and  says  that  such  a  chord 
was  recognized  during  life  by  Schroetter  by  a  peculiar 
musical  note. 

There  was  nothing  striking  in  the  ante-mortem  history 
except  that  the  chest  arched  as  in  rachitis,  and  that  the 
child  was  bluish. 

At  the  end  of  twenty-four  hours  the  child  became  cold, 
and  the  doctor  was  sent  for.     On  his  arrival  it  was  dead. 

Dr.  Kucher  says  that  while  foetal  endocarditis  is  not 
uncommon,  tricuspid  stenosis  is  very  rare.  Rauchfuss 
found  only  two  similar  cases  on  record  ;  one  reported  by 
Peacock  and  one  by  Romberg.    In  Romberg's  case,  a  boy 


194  VALVULAR  DISEASE. 

of  four  years,  the  opening  was  very  narrow,  and  the  tri- 
cuspid valve  had  disappeared.  In  Peacock's  case,  a  girl 
of  seveo  months,  the  stenosis  was  not  considerable,  and 
was  apparently  due  to  the  thickened  valves  with  inflam- 
matory deposits  on  their  outer  walls.  There  were  two 
defects  in  the  intraventricular  septum. 

Tricuspid  and  Mitral  Stenosis. — At  a  meeting  of  the 
London  Pathological  Society  Dr.  Bedford  Fenwick* 
showed  a  specimen  of  tricuspid  stenosis  from  a  woman 
aged  thirty,  who  had  rheumatic  fever  at  fifteen  and  after- 
wards suffered  from  winter- cough  and  dyspnoea.  There 
was  marked  distention  of  the  jugular  veins,  but  no  cya- 
nosis, cardiac  dulness  extending  far  to  the  right,  a  well- 
marked  presystolic  apex  thrill,  and  systolic  and  presys- 
tolic apex  murmur,  to  the  right  another  systolic  and  pre- 
systolic murmur.  At  the  post-mortem  examination  both 
auricles,  but  particularly  the  right,  were  very  much 
dilated,  the  ventricles  small.  The  tricuspid  and  mitral 
valves  were  greatly  thickened,  shortened  and  agglu- 
tinated. Cases  of  this  kind  are  now  known  not  to  be 
very  rare.  Since  his  table  of  forty-six  cases  he  had  been 
able  to  collect  twenty-three  more,  twenty  of  whom  were 
in  females,  average  age  31.7  years.  In  every  case  the 
mitral  valve  was  more  changed  than  the  tricuspid,  and  in 
all  the  general  health  had  been  good.  The  great  dilata- 
tion of  the  right  auricle  caused  increase  of  dulness  to  the 
right,  and  afforded  a  means  of  diagnosis. 

Dr.  Vohsen  f  finds  that  in  nearly  one  half  of  the  chil- 
dren  suffering  from  acute  articular  rheumatism  endocar- 
ditis occurs  and  results  in  marked  valvular  insufficiency. 
The  mitral  valve  was  most  frequently  attacked.  Endo- 
carditis  appears    usually   in   the    first    or   second  week. 


*  The  Medical  Record,  Jan.  20,  1883. 
t  Ibid. 


VALVULAR  DISEASE.  I95 

Pericarditis  is  also  a  frequent  complication.  Salicylate 
of  soda,  while  it  exerts  a  favorable  influence  on  the  joint 
disease,  seems  not  to  prevent  the  cardiac  complications. 
The  mild  forms  of  articular  rheumatism  are  especially 
liable  to  be  followed  by  cardiac  disease. 

Dr.  O'Hara  reported  to  the  Pathological  Society  of 
Philadelphia,*  the  casQof  a  patient,  a  laborer  thirty  years 
of  age.  At  first  the  usual  symptoms  of  cardiac  disease. 
On  admission,  with  the  forearms  flexed  to  a  right  angle, 
the  brachial  arteries  became  prominent  with  each  impulse 
of  the  heart ;  the  pulsations  of  the  carotids  were  wavy  and 
prolonged  ;  the  temporals  were  tortuous  and  pulsated  vis- 
ibly;  no  retinal  arterial  pulsation  was  seen.  Retinal  ven- 
ous pulse  was  marked,  but  venous  pulse  was  found  else- 
where. In  the  second  left  intercostal  space  a  systolic 
impulse  was  observed.  The  pulse  struck  the  finger  with 
considerable  force,  but  at  once  lost  most  of  its  volume. 
This  was  exaggerated  by  raising  the  hands  above  the 
head.  No  hepatic  pulsation  was  felt  over  the  second 
right  costosternal  articulation,  the  closure  of  the  aortic 
valves  was  distinctly  heard  and  a  slight  diastolic  murmur. 
A  systolic  murmur  was  also  heard  over  the  same  spot. 
The  systolic  murmur  was  nearly  lost  in  the  carotid  and 
sub-clavian  arteries. 

The  aortic  valves  were  insufficient  and  thickened  ;  the 
posterior  leaflet  was  normal  in  shape,  but  the  others  were 
curled  on  themselves  on  the  aortic  side.  The  stenosis 
was  slight.  The  mitral  orifice  was  buttonhole  shape,  and 
the  valves  failed  to  close  on  account  of  calcareous  deposit 
in  their  tissue,  extending  into  the  auricle.  Attached 
to  the  valve  a  bony  substance  hung  into  the  ventricle 
one  eighth  of  an  inch  in  diameter.  The  left  auricular 
appendix  was  much  hypertrophied.     The  valves  of  the 

*  N.  V.  Med,  Jour.,  Jan.  20,  1883. 


196  VALVULAR  DISEASE. 

tricuspid  and  pulmonary  orifices  were  normal.  The  pul- 
monary artery  was  considerably  dilated.  Dr.  Eskridge 
thought  that  the  demonstration  of  the  left  auricular  pul- 
sation was  important,  as  Dr.  Broadbent  had  so  recently 
advanced  an  opposite  view :  ( Was  there  a  functional 
murmur  in  the  pulmonary  opening  due  to  enlargement 
of  the  artery?) 

Dr.  Bruch  said  that  he  would  like  to  go  on  record 
among  those  who  had  observed  auricular  pulsation  in 
cases  of  mitral  obstruction,  in  which  the  stenosis  was  ex- 
treme. 

Trtwipet  Bruit. — Dr.  Eskridge  said  that  Hayden  *  re- 
ferred to  bony  deposits  in  the  aorta  and  its  valve  as  fol- 
lows :  Sir  Dominic  Corrigan  exhibited  before  the  Patho- 
logical Society  of  Dublin  (Proceedings,  vol.  ii.,  new  series, 
Feb.,  1864)  the  heart  of  a  young  woman,  in  which  the 
root  of  the  aorta  had  undergone  osteoid  transformation ; 
it  was  likewise  greatly  dilated,  and  the  aortic  valves  had 
been  rendered  thereby  inadequate.  During  the  patient's 
last  illness  a  systolic  murmur  of  metallic  quality, 
appropriately  designated  a  '  trumpet  bruit,*  was  audible 
at  the  base  and  in  the  ascending  aorta  and  carotid  arteries. 
There  was  likewise  a  soft  diastolic  murmur.  He  regards 
a  "  trumpet  bruit*'  as  absolutely  diagnostic  of  bony  de- 
posit in  the  aorta,  either  in  the  form  of  a  ''  rim  of  bone," 
of  a  projection,  or  "tongue  of  bone."  In  the  same  para- 
graph Corrigan  refers  to  Dr.  Banks'  specimen  of  a 
tongue  of  bone  projecting  into  the  aortic  orifice. 

Lying-in  Murmurs  of  the  Heart. — Dr.  Angel  Money  f 
publishes  a  paper  on  this  subject,  the  chief  conclusions  of 
which  are  the  following.  One  kind  is  endocardial-like, 
and  may  be  heard  over  any  part  of  the  precordia.     The 

*  Diseases  of  the  Heart  and  Aorta.     Vol.  ii.,  p.  839. 
\  Medico-Chirurgical  Transactions,    Vol.  65,  1882.         ' 


VALVULAR   DISEASE.  1 97 

second  is  friction-like  and  not  conducted  just  above  and 
to  the  left  of  the  xiphoid  cartilage.  The  third  is  very 
loud,  of  curious  quality,  not  conducted,  and  very  capri- 
cious. Some  of  these  murmurs  occur  in  seventy-five  per 
cent  of  the  lying-in,  and  a  large  part  of  them  are  heard 
over  the  right  heart.  These  murmurs  are  for  the  most 
part  functional  murmurs  and  need  not  excite  any  alarm. 
Relative  Stenosis  of  the  Cardiac  Orifices. — A  theoretical 
explanation  of  the  transient  heart  murmurs  has  been 
advanced.*  In  the  normal  heart,  the  size  of  the  orifice 
multiplied  by  the  velocity  of  the  blood-current  must 
equal  the  cubic  contents  of  the  heart  cavity.  If  the 
latter  be  greater,  we  have  stenosis.  Hitherto  but  one 
factor  has  been  taken  into  account,  viz.,  the  diameter 
of  the  orifice,  but  it  is  clear  that  if  with  a  normal  exit  the 
capacity  of  the  heart  be  increased,  the  former  becomes 
relatively  too  small,  and  we  have  a  relative  stenosis.  The 
auriculo-ventricular  opening  partakes  in  the  dilatation  of 
the  cavities,  to  the  extent  indeed  that  the  unchanged 
valves  become  too  small,  and  insufficiency  results.  But 
the  arterial  orifices  do  not  dilate  as  the  ventricles  enlarge 
and  hence  become  too  small.  As  regards  the  third  factor — 
the  velocity  of  the  blood-current — a  certain  relation  exists 
between  the  capacity  of  the  heart  and  the  size  of  its  ori- 
fices, which  permits. changes  in  the  velocity  of  the  current 
within  certain  limits.  But  when  through  congenital  de- 
fect or  in  consequence  of  pathological  changes  the  ven- 
tricle can  barely  empty  itself,  a  slight  increase  in  the 
velocity'will  produce  a  murmur.  On  the  other  hand,  a 
pre-existing  murmur  may  disappear  on  the  retardation  of 
the  blood  current.  Witness  the  disappearance  of  a  sys- 
tolic murmur  after  a  severe  hemorrhage.  We  should 
make  a  distinction  between  organic  and  functional  or 
clinical  stenosis.    Organic  valvular  changes  are  sometimes 

*  The  Med.  Record,  Sept.  23,  1882. 


198  VALVULAR  DISEASE. 

found  after  death  that  gave  rise  to  no  murmurs  during 
life.  In  acute  endocarditis  or  during  a  high  fever,  there 
may  be  a  weakening  of  the  muscular  walls  of  the  heart 
and  consequent  dilatation.  Here  the  relation  between 
the  ventricle  and  its  orifice  is  altered,  and  the  latter  be- 
comes stenosed.  The  sound  produced  is  a  blowing  mur- 
mur, heard  oftenest  and  loudest  over  the  left  heart,  and 
of  course  systolic.  After  copious  hemorrhage  loud  blow- 
ing systolic  murmurs  arise,  often  not  till  the  vessels  are 
refilled  by  the  absorption  of  the  water  of  the  tissues. 

From  insufficient  nutrition,  the  muscular  tone  of  the 
heart  is  lowered  and  there  is  consequent  dilatation.  When 
this  condition  exists,  the  orifice  being  relatively  too  small 
for  the  ventricle,  only  a  part  of  the  contents  of  the  latter 
can  pass  out ;  the  balance  recoiling  against  the  advancing 
blood-stream  causes  a  murmur. 

Before  proceeding  with  the  consideration  of  the  treat- 
ment of  valvular  disease,  I  append  a  letter,  in  which  my 
opinion  is  asked  regarding  the  relation  between  heart  and 
kidney  lesions,  and  the  reply,  in  which  are  set  forth  the 
views  I  have  entertained  upon  this  subject  for  many  years. 

Springfield,  Vt.,  Aug.  20,  1883. 
Prof,  Alonzo  Clark,  M.D. 

Dear  Sir  :  The  following  case  reported  at  a  local 
medical  society  excited  some  interest  among  the  mem- 
bers, and  it  would  be  gratifying  to  them  to  know  your 
opinion  of  it.  Is  it  possible,  do  you  think,  to  decide 
which  is  the  initial  lesion  when  the  heart  and  kidneys  are 
involved  (as  in  this  case)  by  the  clinical  history,  and  by 
the  stage  of  development  of  each  lesion,  as  shown  by  the 
autopsy?  If  it  would  not  encroach  too  much  upon  your 
time,  would  you  have  the  kindness  to  give  us  your 
opinion  T  With  high  esteem, 

I  am,  very  respectfully,  yours, 
Daniel  W.  Hazelton. 


VALVULAR   DISEASE.  1 99 

Case. — Nov.    1880.      J.    B.,  male;    age    72;    married; 
farmer  by  occupation,  and  a  man  of  good  habits.     When 
first  seen  he  gave  a  history  of  repeated  attacks  of  acute  ar- 
ticular rheumatism  during  the  preceding  20  years.     For 
a  long  time  he  had  had  dyspnoea,  which  was  made  worse 
by   exertion.      The    dyspnoea   persisted    and    was    more 
marked  than  ever  before.      For  days  he  was  unable  to 
maintain  any  but   the  sitting   posture.     Pulse  was  inter- 
mittent.    There  was  a  cough  and  expectoration  occasion- 
ally streaked  by  blood.     There  was  fulness  of  the  super- 
ficial veins  of  the  neck,  and  distinct  pulsation  of  the  jug- 
ulars.  Lower  extremities  were  oedematoeus,  auscultatation 
gave  a  systolic   murmur  heard   best  at  the  apex   of  heart 
and  indistinctly  at    angle  of  scapula.     Percussion  showed 
the  area  of  cardiac   dulness   to  be  increased,    extending 
from  J  to  I  inch  farther  to  right  of  sternum  than  normal. 
Urine  on  first  examination  and  for  some  time  subsequently 
was  about  natural  in  quantity  and  color ;  specific  gravity 
about  1015,  and  contained  a  truce  of  albumen.     At  dif- 
ferent times  during  the  succeeding  year  the  patient  had 
small  hemorrhages   from    the  lungs,  and  at  various  times 
the  lungs  gave  dulness  on  percussion,  when  dyspnoea  was 
increased.      He  also  had   hemorrhages  from    the  bowels, 
one  of  which  was  profuse.     Patient  died    with  symptoms 
of  uraemia  and   pericarditis  December,  1882.     Autopsy: 
Pericardium  congested  and  bound  by  recent  adhesions  to 
heart.     Heart  was  moderately  dilated.  Right  side  more 
dilated  than  left.  Left  side  about  normal — weighed  22  oz. 
Mitral  valve  had   an  abundant  deposit  on  it  of  calcareous 
matter,  also  the  margins  of  the  auriculo-ventricular  orifice. 
The  kidneys  were  slightly  atrophied.     Their  capsules 
were  easily  removed.  One  cyst  about  the  size  of  a  pea  was 
found  between  the  capsule  and  cortex  of  one  kidney.  They 
were  of  about  the  natural  reddish  color,  but  were  studded 
with  very  fine  and  rather  indistinct  millet  seed  granulations. 


200  VALVULAR  DISEASE. 

On  section,  the  cortex  and  pyramids,  presented  their 
natural  color  and  structure  so  far  as  the  unaided  eye 
could  determine.  The  cortices  were  not  diminished  in 
breadth.     Other  viscera  were  normal. 

*'  Dear  Doctor  : 

"It  has  been  the  subject  of  much  discussion,  when  car- 
diac and  renal  disease  are  found  in  the  same  patient,  which 
preceded.  This  question,  in  my  mind,  divides  itself  into 
two,  and  would  be  answered  as  follows :  When  it  is  the 
large  kidney,  with  albumen  and  casts  in  the  urine  and 
much  oedema  during  life,  then  in  nine-tenths  of  the  cases 
the  heart  disease  is  primary  and  the  kidney  affection  is 
secondary  and  consequent.  When,  on  the  other  hand, 
the  kidney  is  contracted,  and  during  life  the  albumen  is 
scanty  and  often  absent,  the  casts  are  uncertain,  there  is 
but  little  oedema,  and  there  is  no  distressing  valvular  dis- 
ease, then  the  chances  are  at  least  even  that  the  renal 
disease  is  primary. 

**  In  your  case  the  articular  rheumatism  had  been  re- 
curring for  twenty  years,  and  "  for  a  long  time  the  pa- 
tient had  had  dyspnoea."  How  long  ?  This  question  is 
important.  If  he  was  pretty  well  and  could  attend  to 
his  business  for  six  months  or  for  some  years  after  the 
rheumatic  attack  or  attacks,  and  then  the  difficulty  of 
breathing  came  slowly,  with  perhaps  at  times  an  urgent 
attack,  and  if  especially  this  difficulty  increased  rapidly 
after  the  oedema  appeared,  then  you  have  the  history  of 
rheumatic  mitral  disease  as  the  primary  affection  and  the 
renal  is  secondary. 

"  In  your  case  there  was  calcareous  deposit  on  the  mitral 
valve  and  in  the  margin  of  the  orifice.  That  means  years. 

"  Then,  again,  *'  the  left  side  of  the  heart  was  about  nor- 
mal," the  right  was  dilated,  and  the  heart  weighed  22  oz. 
It  is  evident,  then,   that  there  was  hypertrophy  some- 


VALVULAR  DISEASE.  20I 

where-  It  was  not  in  the  left  side.  There  must  have 
been  hypertrophy  with  the  dilatation  of  the  right  side. 
This  should  be  looked  for  because  of  the  long  standing 
stenosis  of  the  mitral  valve.  You  do  not  state  that  there 
was  a  diastolic  mitral  murmur.  Yet,  from  the  hypertro- 
phy of  the  right  ventricle  and  the  condition  of  the  mi- 
tral valve  and  orifice,  I,  infer  that  it  did  exist  at  one  time 
and  had  been  lost  as  the  strength  of  the  heart  diminished 
toward  the  end  of  life. 

'^  Then  as  to  the  kidneys.  They  do  not  appear  to  have 
been  in  a  state  of  advanced  disease.  They  were  "  slight- 
ly atrophied."  They  were  finely  granulated,  but  their 
capsules  were  not  unnaturally  adherent,  while  the  internal 
structures  were  not  perceptibly  changed.  There  was  one 
serous  cyst,  but  only  one,  and  that  was  small.  This  ap- 
pears to  be  the  early  stage  of  the  contracted  kidney,  a 
disease  which  sometimes  reduces  the  weight  of  the  organ 
to  one  and  a  half  ounces. 

"  When  the  small  kidney  produces  disease  of  the  heart 
it  is  the  left  side  that  is  affected  and  hypertrophy  is  asso- 
ciated with  it,  or  it  is  hypertrophy  alone.  In  my  judg- 
ment, then,  the  chronic  disease  of  heart  antedates  the 
disease  of  the  kidney,  but  probably  was  not  the  cause 
of  it.  The  contracted  kidney  is  not  that  which  usually 
follows  cardiac  disease,  but  the  large  one.  How  a  kidney 
of  the  kind  you  have  described  should  have  occurred  in 
such  a  case  is  a  problem  I  cannot  solve.  If  it  was  really 
produced  by  the  heart  it  is  a  noteworthy  exception  to  the 
rule  I  have  referred  to.  If  it  was  the  result  of  the  unknown 
agencies  which  usually  produce  the  contracted  kidney^ 
even  then  the  concurrence  is  worth  remembering.  One 
other  supposition  is  possible.  The  influences  that  pro- 
duce the  contracted  kidney  may  have  been  operative  be- 
fore the  dyspnoea  was  experienced  and  when  that  came, 
the  congestive  state  of  the  kidneys,  which  comes  with  it, 


202  VALVULAR  DISEASE. 

may  have  counteracted  the  contraction  and  suspended  it. 
Whether  this  is  possible  I  do  not  know,  '  If  it  is,  then 
whether  it  explains  this  case  can  be  better  judged  of  when 
we  know  for  how  many  of  the  twenty  years  the  dyspnoea 
existed.  The  duration  of  the  cirrhotic  kidney  may  never 
be  known,  but  after  it  is  recognizable  the  patient  often 
lives  three  or  four  years.  Still  it  is  difficult  to  suppose 
that  it  can  have  a  total  duration  of  twenty  years. 

"  There  is  one  other  point  in  the  case.  Your  patient 
had  pericarditis  at  the  end.  You  state  that  the  urine  con- 
tained a  little  albumen,  and  your  idea  that  he  was  also 
uraemic  is  altogether  probable.  This  state  of  the  blood 
is  quite  capable  of  producing  pericarditis  and  probably 
did  in  your  case. 

"  The  other  points  in  your  case  are  easily  explained. 
The  cough,  the  expectoration,  and  the  blood  stains  were 
produced  by  the  distention  of  the  vessels  consequent 
on  the  mitral  regurgitation  and  stenosis.  The  intestinal 
hemorrhage  from  the  overloaded  state  of  the  right  heart 
and  its  unwillingness  to  receive  the  blood  of  the  hepatic 
and  portal  vessels  and  the  consequent  rupture  of  some 
intestinal  veins.  The  fulness  of  the  veins  in  the  neck  and 
the  pulsation  in  the  jugulars  were  due  to  regurgitation 
through  the  tricuspid  opening,  for  while  the  right  ventri- 
cle was  dilated  its  auriculo-ventricular  opening  would  be 
enlarged  also,  and  so  render  the  valve  insufficient  to 
guard  it. 

*^  You  say  '  at  various  times  the  lungs  gave  dulness  on 
percussion,'  but  you  do  not  state  in  what  part  of  the  chest 
this  dulness  was  found,  or  whether  it  was  on  both  sides. 
If  it  was  on  both  sides  and  in  the  lower  part  of  it,  it  was 
dependent  on  double  pleural  serous  effusion — an  event 
not  uncommon  in  cardio-renal  disease.  It  is  a  part  of  the 
dropsy  not  caused  by  inflammation,  and  it  is  therefore 
painless,  but  it  greatly  embarrasses  the  respiration.    It  is 


VALVULAR  DISEASE.  203 

possible  for  congestion  of  the  vessels  of  the  lungs  to  so 
far  exclude  the  air  from  the  air  cells  as  to  make  dulness. 
This,  is  however,  somewhat  peripatetic,  moving  from 
place  to  place  in  the  lung  or  from  one  lung  to  the  other 
and  is  apt  to  be  attended  by  haemoptysis. 

"  Finally,  you  appear  to  have  found  no  fluid  in  the  peri- 
cardium only  lymphy  adhesions,  yet  you  found  percus- 
sive dulness  on  the  right  of  the  right  edge  of  the  sternum 
one  half  to  an  inch  in  extent.  This  was  probably  due  to 
a  serous  effusion  in  the  pericardium  that  was  absorbed 
before  death." 


204  TREATMENT  OF  VALVULAR  DISEASE. 


LECTURE  XIII. 

PROGNOSIS  AND  TREATMENT  OF  VALVULAR  DISEASE. 

In  regard  to  the  treatment  of  valvular  disease,  it  is 
so  entirely  bound  up  in  the  subject  of  treatment  of 
cardiac  diseases  in  general  that  it  does  not  require  atten- 
tion at  this  time.  The  question  will  naturally  occur  to 
you,  how  much  havoc  can  be  made  by  these  diseased 
valves  ?  How  dangerous  is  it  ?  The  reply  would  be  this  : 
Obstruction  at  the  aortic  opening  is  the  least  dangerous 
of  all,  because  of  the  compensation  that  can  be  furnished 
by  hypertrophy  of  the  heart.  Obstruction  at  the  mitral 
opening  will  be  grave  or  not,  depending  upon  its  extent. 
As  I  told  you,  one  day  it  may  become  a  very  grave  matter, 
producing  cyanosis  that  may  be  visible  in  the  face,  a  con- 
gestion of  all  the  important  organs  of  the  body,  and  lead- 
ing to  rather  a  slow  death,  that  is,  an  illness  that  may  be 
protracted  through  several  months,  or  half  a  year,  or  even  a 
year,  and  finally  terminating  in  death.  But  diseases  of  the 
mitral  valve  usually  have  a  slow  ending  through  affections 
of  the  kidneys  and  dropsy,  particularly  oedema.  Regur- 
gitation at  the  mitral  valve  goes  in  the  same  class  ;  it  stands 
with  obstruction  of  the  mitral  valve  in  regard  to  its  mode 
of  termination  ;  that  form  of  disease  that  is  most  likely 
to  have  a  sudden  termination,  that  condition  in  which  the 
patients  are  sometimes  told  they  may  drop  down  dead  in 
a  moment ;  and  this  is  a  very  unwise  thing  to  tell  a  patient ; 
it  makes  him  anxious  all  his  life,  fearing  at  every  moment 
he  may  drop  down  dead.  The  condition  that  is  most 
likely  to  be  attended  by  this  sudden  result  is  regurgitation 


TREATMENT   OF  VALVULAR  DISEASE.  20$ 

at  the  aortic  opening,  by  a  return  of  blood  into  the  ven- 
tricle after  it  has  once  entered  the  aorta.  You  can  easily 
see  that  in  this  case,  depending  upon  how  much  regurgi- 
tation there  is,  there  will  be  a  diminished  quantity  of 
blood  circulating  in  the  arteries  of  the  body.  The  brain 
will  not  receive  its  due  amount,  and  syncope  may  take 
place,  you  cannot  say  \yhen.  It  does  not  require  a  very 
grave  lesion  of  this  kind  to  lead,  in  certain  instances,  to 
sudden  death,  and  it  almost  always  occurs  by  a  sort  of 
syncope,  the  brain  receiving  too  little  blood  to  stimulate 
it  to  proper  action,  and  to  react  upon  the  heart.  The 
heart  ceases  to  beat  and  the  patient  is  dead.  And  yet 
do  not  give  these  patients  unnecessary  alarm.  They  may 
carry  this  lesion  that  leads  to  regurgitation  from  the  aorta 
into  the  ventricle  for  a  great  many  years.  The  number 
of  instances  in  which  persons  die  with  this  lesion  suddenly, 
compared  with  those  who  die  a  lingering  death,  is  very 
small.  It  is  an  old  error  to  suppose  that  persons  who 
have  cardiac  disease  must  die  suddenly.  They  may,  and 
others  may.  A  good  many  years  ago,  when  I  was  just 
entering  upon  the  profession,  I  took  up  the  study  of  the 
cause  of  sudden  deaths  ;  and  one  of  the  first  that  occurred 
which  I  studied  was  of  a  young  woman  in  Bellevue  Hos- 
pital. She  had  had  typhus  fever.  It  was  in  1847.  I 
was  not  so  young  in  the  profession  as  I  was  thinking. 
Well,  typhus  fever  was  prevailing  there  to  a  remarkable 
extent.  She  had  got  through  with  her  typhus  fever,  and 
was  in  a  condition  of  convalescence.  She  was  able  to  go 
about  the  wards  and  take  care  of  other  patients  to  a  cer- 
tain extent,  but  she  felt  a  little  weary  at  times.  After 
eating  dinner  she  had  lain  down  upon  her  bed  and  taken 
a  nap.  Another  patient,  her  next  neighbor,  had  done 
the  same  thing.  She  woke  from  her  nap,  raised  herself 
in  bed,  and  said  to  her  neighbor,  '*  I  have  not  felt  so  well 
as  I  do  at  this  moment  since  I  was  first  taken  sick,"  and 


2o6  TREATMENT  OF  VALVULAR  DISEASE. 

had  scarcely  finished  the  sentence  when  she  fell  back 
senseless,  dead.  At  post-mortem  examination  we  found 
there  was  an  effusion  of  blood  at  the  base  of  the  throat,  in- 
volving all  the  nerves  of  respiration,  compressing  them  to  a 
certain  extent,  so  that  the  respiration  stopped  suddenly. 
In  following  up  the  inquiry,  I  found  within  six  months  six 
cases  of  the  same  kind.  Since  then  I  have  not  seen  one. 
Sudden  death,  then,  has  a  variety  of  causes.  In  a  person 
who  is  known  to  have  cardiac  disease  it  is  usually  ascribed 
to  that  affection,  but  it  is  not  a  matter  of  course  that  it 
will  be  so.  And  then  you  are  to  bear  in  mind  that  in 
certain  forms  of  disease  of  the  heart  there  is  greater  dan- 
ger at  the  brain  than  there  is  at  the  heart  itself.  That  is, 
hypertrophy  of  the  heart  without  obstruction  is  a  rather 
frequent  cause  of  apoplexy.  An  hypertrophy  of  the  heart 
without  obstruction  between  the  arteries  of  the  brain  and 
the  heart  itself  is  apt  to  lead  to  apoplexy. 

/;/  Regard  to  Remedies. — In  cases  of  dizziness  from  heart 
disease,  See*  asserts  that  iron  *is  absolutely  indicated, 
though  in  many  cases  the  iodide  of  potass  gives  excellent 
results. 

Anginous  attacks  should  of  course  be  combatted  by 
hypodermics  of  morphine,  the  administration  of  chloral, 
or  the  inhalation  of  nitrite  of  amyl  during  the  access, 
and  by  the  bromide  of  potassium  and  digitalis  or  con- 
vallaria  during  the  intervals. 

Excellent  results  are  claimed  in  the  treatment  of  car- 
diac dropsy  by  caffein.  Begin  with  a  dose  of  7  grains, 
gradually  increasing  to  15,  30,  and  even  45  grains  per 
diem.  Such  large  doses,  however,  often  cause  severe 
pain  in  the  stomach. 

Adonis  vernalis\   has    long    been   used   as  a   dropsy 

^  Med.  Rec.  Sept.  22,  1883. 

\  The  Medical  Record,  Oct.  6,  1883. 


TREATMENT  OF  VALVULAR  DISEASE.  20; 

remedy  in  Southern  Russia,  and  Prof.  Bolkin  has  em- 
ployed it  extensively,  and  Dr.  Budnoff  reports  the  result. 
It  was  found  to  be  of  value  only  in  the  dropsies  that  were 
preceded  by  cardiac  disease.  The  heart-beats  were  much 
strengthened.  The  size  of  the  organ  was  diminished,  and 
its  tones  were  much  louder.  The  systolic  murmur  of 
aortic  stenosis  especi^illy  was  intensified.  The  heart's 
rhythm  became  more  regular,  and  the  pulse  slower  and 
fuller.  The  daily  excretion  of  urine  was  increased  greatly, 
sometimes  rising  from  ten  or  twelve  to  eighty  or  ninety, 
ounces  a  day.  The  subsidence  of  oedema  was  propor- 
tioned to  the  flow  of  urine.  The  medicine  was  given  in 
infusion  of  the  strength  3  i.  to  |  vi.,  to  which  two  drops  of 
the  oil  of  peppermint  was  added.  The  dose  of  this  was 
a  tablespoonful  every  two  hours. 

Dr.  Bubnow"^  of  St.  Petersburg,  says  that  it  is  a  popu- 
lar remedy  in  Russia  for  dropsy.  Under  its  influence  the 
cardiac  contractions  are  increased  in  force  and  diminished 
in  frequency,  and  the  urine  was  augmented,  and  no  longer 
contained  casts  or  albumen.  Experiments  on  both  cold 
and  warm-blooded  animals  with  different  preparations 
(infusion,  aqueous  and  alcoholic  extracts),  showed  that  its 
action  is  to  stimulate  both  the  motor  ganglia,  and  the 
imbibitory  apparatus  of  the  heart,  and  to  raise  arterial 
tension.  Dr.  Bubnow  prefers  adonis  to  digitalis,  and  says 
that,  like  convallaria,  it  has  no  cumulative  action.  A  glu- 
coside  adonidin  containing  the  active  principle  has  been 
isolated.  The  effects  of  adonidin  are  very  similar  to 
those  of  digitalin.  It  is  not  improbable  that  the  same 
similarity  may  be  found  to  exist  between  adonis  and 
digitalis  as  exists  between  hyoscyamus  and  belladonna. 

The  therapeutic  uses  of  convallaria  are  thus  stated  by 
Prof.  Seef : 

*N.  Y.  Med.  Jour.,  June  i6,  1883. 
\Ain.  Jour,  of  Med.  Sci.,  Oct.,  1882. 


208  TREATMENT  OF  VALVULAR  DISEASE. 

1.  In  palpitation  due  to  an  exhaustion  of  the  vagus 
nerve  or  paralytic  palpitation. 

2.  In  simple  want  of  rhythm  with  or  without  hypertro- 
phy, with  or  without  lesions  of  orifices  or  valves. 

3.  In  mitral  stenosis  the  contractile  power  is  increased 
as  shown  by  the  sphygmograph. 

4.  In  insufficiency  of  the  mitral  valve,  particularly  when 
there  is  passive  congestion  of  the  lungs  and  consequent 
dyspnoea. 

5.  In  aortic  regurgitation  (Corrigan's  disease)  the  good 
effects  are  shown  in  the  pulse  and  easier  respiration.  It 
gives  strength  and  energy  to  the  heart. 

6.  In  dilatation,  w4th  or  without  hypertrophy ;  with 
or  without  fatty  degeneration ;  with  or  without  sclerosis 
of  the  muscular  tissue. 

7.  In  all  cardiac  affections  giving  rise  to  dropsy  and 
anasarca  surpassing  all  other  drugs. 

The  combination  of  convallaria  with  the  iodide  of  po- 
tassium is  most  valuable  in  cardiac  asthma. 

In  the  Medical  Record  for  Feb.  24,  1883,  may  be  found 
the  report  of  twenty-one  cases  treated  with  this  drug,  all 
heart  disease  in  some  form ;  the  ages  of  the  patients  from 
eleven  to  seventy  years. 

The  preparation  was  an  infusion  3  ^  to  |  i.  to  a  pint,  in 
tablespoonful  doses  every  two  hours.  In  seventeen  cases 
there  were  absolutely  no  results,  and  in  the  others  the  im- 
provement was  trifling.  The  writer  therefore  does  not 
admit  that  convallaria  is  an  efficient  substitute  for  digita- 
lis. He  does  admit,  however,  that  the  specimens  of 
convallaria  used  by  him  may  have  been  of  a  quality  infe- 
rior to  that  used  by  other  observers,  who  have  reported 
such  brilliant  results. 

Dr.  B.  Robinson*  exhibited  to  the  N.  Y.  Pathological 

*  The  Medical  Record,  Jan.  13,  1883, 


TREATxMENT   OF  VALVULAR  DISEASE.  209 

Society  the  hearts  and  kidneys  of  two  persons  who  were 
similarly  affected,  and  in  whom  both  digitalis  and  con- 
vallaria  were  equally  ineffectual  in  producing  diuresis,  in 
both  of  whom  the  contracted  kidney  was  found,  regard- 
ing which  Dr.  Robinson  expresses  the  following  opinion: 
*'  We  should  be  prepared  to  assume  that  with  a  small 
quantity  of  urine,  with, nothing  specially  abnormal  about 
the  specific  gravity,  and  failure  on  the  part  of  the  kidneys 
to  respond  to  cardiac  stimulants,  as  in  the  case  recited, 
we  might  reasonably  expect  to  find  that  form  of  kidney 
degeneration." 

Dr.  A.  A.  Smith's*  experience  with  convallaria  had  led 
him  to  think  it  a  good  diuretic.  It  had  seemed  to  him 
that  in  cardiac  hypertrophy  the  remedy  was  not  indicated. 
In  chronic  renal  disease,  with  chronic  hypertrophy,  ac- 
cording to  his  observations,  it  aggravated  the  symptoms. 

In  cases  of  enlargement  of  the  heart  in  which  dilatation 
predominates  it  serves  a  very  good  purpose.  He  was  not 
however,  prepared  to  give  up  digitalis,  and  substitute 
convallaria.  Nor  was  he  quite  sure  the  experiments  of 
Ott  had  not  demonstrated  that  it  does  not  act  through 
the  pneumogastric. 

Dr.  Vanderpoelf  found  in  a  case  in  which  there  was 
mitral  stenosis  and  insufficiency  with  irregular  action  of 
the  heart  and  cedema,  that  eight  minim  doses  of  the  fluid 
extract  of  convallaria  twice  a  day  brought  marked  im- 
provement, removed  the  oedema  in  ten  days,  and  brought 
a  more  regular  heart  action. 

Dr.  Delafield  said  it  made  the  heart  action  more  regular 
and  slower  in  certain  cases,  and  in  general  condition  the 
patient  improved  very  much.  He  had  found,  like  Drs. 
Vanderpoel  and  Barker,  that  there  was  a  great  difference 
■ 

*  Medical  Record  Q^.  Y.  Acad,  of  Med.),  April  14,  1883. 

t  N.  Y.  AUd.  Jour.,  Apr.  14,  1883.    (N.  Y.  Med.  and  Surg.  Soc.) 


2IO  TREATMENT    OF   VALVULAR   DISEASE. 

in  patients  as  to  dose.  For  some  five  drops  of  fluid  ex- 
tract every  three  hours  was  enough,  while  other  patients 
required  drachm  doses.  He  thinks  he  saved  the  life  of 
a  woman,  over  seventy  years  of  age,  overwhelmed  by 
pneumonia,  with  twenty-drop  doses  of  the  fluid  extract 
every  three  hours. 

Dr.  Hurd"  has  translated  Prof.  Germain  See's  opinions 
of  this  new  medicine,  which  are  mostly  embraced  in  the 
following  extracts  :  In  the  form  of  aqueous  extract  of  the 
entire  plant,  given  in  doses  of  half  a  gramme  to  a  gramme 
and  a  half  daily,  it  produces  on  the  heart  blood-vessels 
and  respiratory  organs,  effects  constant  and  constantly 
favorable,  viz.:  a  slowing  of  the  beatings  of  the  heart, 
with  often  a  restoration  of  the  normal  rhythm,  augmenta- 
tion of  the  energy,  also  of  arterial  pressure,  the  respira- 
tory force  is  increased.  ...  In  all  cardiac  affections  in- 
differently, from  the  moment  the  watery  infiltrations  ap- 
pear, it  has  an  action  prompt  and  certain.  Dr.  Hurd  has 
tried  the  fluid  extract  in  doses  of  five  drops  every  four 
hours  in  two  cases  with  very  satisfactory  results. 

Dr.  Troitsky  t  says  it  may  be  used  to  make  the  heart's 
contractions  stronger,  slower,  and  more  regular,  especially 
in  cases  of  organic  disease,  or  those  in  which  increased  fre- 
quency depends  on  changes  in  the  nerve  centres ;  to 
lower  the  temperature  so  far  as  its  influence  on  the 
heart  may  permit ;  to  increase  arterial  tension ;  to  in- 
crease the  secretion  of  urine  in  dropsy ;  to  lower  reflex 
action.  He  says  that  it  acts  better  in  mitral  regurgitation 
than  in  the  diseases  of  the  aortic  valve  and  mitral  ste- 
nosis. In  this  respect  it  is  like  digitalis — ten  or  twelve 
grains  of  the  flowers  to  six  ounces  of  water,  three  or  four 
tablespoonfuls  a  day.     Convallaria  in  large  doses  does  not 

*The  Medical  Record,  Sept.  9,  1882. 
\  N.  Y.  Med.  Abstract,  April,  18S3. 


TREATMENT   OF  VALVULAR  DISEASE.  211 

stimulate  the  cardiac  terminations  of  the  vagi — does  not 
stimulate  the  cardiac  nerves.  It  stimulates  the  central 
inhibitory  apparatus.  It  paralyzes  the  motor  centres 
situated  within  the  heart  itself.  It  at  first  accelerates 
then  retards  the  respiration,  and  finally  stops  it  just 
after  the  heart  has  stopped,  and  he  thinks,  because  the 
respiratory  centres  are  paralyzed  by  the  venosity  of  the 
blood.  Temperature  at  first  rises  half  to  one  degree  C, 
then  falls  considerably  because  it  paralyzes  the  vaso- 
motor centres.  It  first  stimulates  then  paralyzes  the 
vaso-motor  centres,  hence  increased  and  then  diminished 
vascular  tension.  On  the  brain  it  produces  anaemia  and 
sleep  ;  applied  directly  to  striated  muscle  the  extract  pro- 
duces complete  loss  of  contractility. 

The  trial  of  this  drug  in  the  Roosevelt  Hospital,  under 
the  direction  of  Dr.  Delafield,  reported  by  Dr.  Taylor,"^ 
is  summed  up  as  follows :  "  Of  the  five  cases  of  cardiac 
disease  four  improved — one  veiy  markedly — after  digitalis 
had  failed ;  one  improved  at  first,  then  grew  very  much 
worse  and  recovered  on  digitalis.  One  was  hopeless. 
Case  XL,  already  referred  to,  was  as  brilliant  an  example 
of  the  benefit  to  be  derived  from  a  drug  in  certain  in- 
stances as  I  saw  during  my  hospital  experience."  Fifteen 
other  cases  are  reported  in  which  the  medicine  was  used 
in  other  diseases.  One,  a  case  of  pneumonia,  hardly  a 
less  brilliant  illustration  of  the  power  of  the  medicine  than 
the  Case  XI.  of.  heart  disease.  The  fluid  extract  was 
given  X  minims  three  times  a  day  to  XX  minims  every 
four  hours. 

Dr.  Polkf  reported  to  the  Practitioners'  Society  a  case 
of  palpitation  in  which  the  heart  would  beat  240  times  in 
the  minute,  in  one  instance  for  three  days.     Drs.  Polk, 


*The  Medical  Record,  Feb.  13,  1883,  and  a  previous  number, 
flbid,  Feb.  3,  1883. 


212  TREATMENT   OF  VALVULAR  DISEASE. 

Peabody,  Flint,  and  Metcalfe  had  all  failed  to  find  any 
organic  change  in  the  heart.  The  patient  was  a  young 
man  of  twenty  years.  In  one  of  these  attacks  Dr.  Polk 
gave  him  ten  minims  of  the  fluid  extract  of  convallaria 
hypodermically,  and  one  half  hour  later  repeated  it.  Five 
to  ten  minutes  after  this  the  pulse  fell  to  120,  and  fell  not 
gradually,  but  suddenly.  Fifteen-drop  doses  every  three 
hours.  The  next  morning  the  pulse  was  90  in  the  min- 
ute. The  intervals  were  lengthened  to  four  hours,  and 
the  next  day  the  medicine  was  suspended.  There  was 
no  return  of  palpitation. 

Dr.  Beverly  Robinson*  reported  to  the  Practitioners* 
Society  an  eleven  years  old  asthma  in  a  man  sixty- 
three  years  old,  inherited,  which  was  greatly  relieved  by 
the  fluid  extract  of  the  root  of  convallaria.  The  first 
dose  of  fifteen  minims  gave  sensible  relief.  Then  it 
was  four  minims  in  eight  of  syrup  of  tolu  and  water 
sufficient  to  make  a  drachm,  every  three  hours,  then 
five  drops  of  the  extract  every  three  hours.  It  was  con- 
tinued through  December,  having  been  begun  Oct.  4, 
1883. 

Dr.  Ott  finds  that  the  slowing  of  the  heart  by  digitalis 
is  due  to  a  cardiac  inhibitory  excitation  ;  with  convallaria 
some  other  part  of  the  heart  is  acted  on  (he  thinks  the 
muscle).  Digitalis,  as  a  rule,  does  not  primarily  accel- 
erate the  heart ;  convallaria  does.  After  section  of  the 
spinal  cord  digitalis  is  powerless  to  increase  arterial 
tension,  while  convallaria  is  not.  If  we  compare  the 
action  of  the  drug  with  other  cardiac  agents,  as  aconite, 
or  astragalus  molissimus,  it  is  found  that  it  does  not 
belong  to  this  group.  As  these  resemble  each  other  in 
their  action,  yet  many  important  differences  exist.  So 
does  convallaria  differ  from  digitalis  in  several  important 

*  The  Medical  Record,  Feb.  3,  1^83. 


TREATMENT   OF    VALVULAR  DISEASE.  213 

particulars.  The  great  rise  of  arterial  tension  would 
indicate  its  value  in  dropsies.  It  is  a  drug  which  must 
not  be  pushed  to  any  great  extent  for  fear  of  producing 
spasm. 

Salicyl  Compounds  in  Rheumatism. —  Dr.  Maclagen  * 
again  brought  forward  his  views.  He  urges  that  small 
doses  are  ineffectual,  .but  that  we  employ  large  doses  and 
at  frequent  intervals — say  twenty  to  forty  grains  every 
hour  for  six  hours,  or  until  there  is  relief  from  pain.  Dr. 
Maclagen  thinks  that  we  may,  by  the  early  and  free  use 
of  salicin,  prevent  valvular  inflammation.  Dr.  Sansom, 
while  indorsing  much  that  Dr.  Maclagen  has  said,  was 
not  so  sanguine  as  to  the  preventive  action  of  salicin. 

Cactus  GrandifloriLs  in  Heart  Affections.  —  Dr.  M. 
O'Haraf  at  a  meeting  of  the  Philadelphia  County  Medi- 
cal Society  said  that  his  attention  was  first  called  to 
this  cactus  some  time  ago,  and  failing  with  the  usual 
remedies  in  a  case  of  mitral  disease  with  oedema, 
dyspnoea,  etc.,  he  gave  five  minims  of  the  fluid  extract  of 
the  cactus  grandiflorus.  Every  symptom  improved,  and 
in  two  weeks  the  patient  was  quite  another  man.  He 
had  two  other  similar  cases  which  give  similar  evidences 
of  the  virtues  of  the  cactus.  He  says  that  if  he  can 
trust  a  limited  experience  the  cactus  is  a  pure  heart  tonic. 

He  refers  to  various  other  remedies  recommended  by 
different  persons  who  think  that  their  action  is  similar 
to  that  of  digitalis,  but  he  has  not  tried  them. 

Dr.  Finny  :j:  thinks  that  too  much  dependence  may 
be  placed  on  the  physical  signs  of  mitral  regurgitation  as 
evidence  of  organic  disease;  that  such  signs  may  be  due 
to  purely  functional  derangements  and  weakness  of  the 


*The  Medical  Record,  April  7,  1883. 

f  N.  Y.  Medical  Journal,  Nov..  17,  1883. 

X  The  Medical  Record,  March  17,  1883. 


214  TREATMENT   OF  VALVULAR  DISEASE. 

heart,  or  to  an  altered  condition  of  the  blood ;  that  the 
blood  murmurs  in  the  heart  and  large  vessels  may  be 
louder  than  those  produced  by  valvular  lesions;  that  the 
danger  of  valvular  disease  is  enormously  increased  by 
weakness  of  the  cardiac  walls;  that  the  lowering  treat- 
ment of  the  heart's  force  is  rarely  if  ever  required  in  heart 
disease;  that  indications  for  treatment  in  diseases  of  the 
heart  should  be  sought  from  the  evidences  of  the  condi- 
tion of  the  heart  muscle,  and  not  from  those  of  the 
condition  of  the  valves. 

Dr.  Leech*  said  his  general  plan  in  the  treatment  of 
cardiac  dropsy  was  to  place  his  patient  in  bed,  secure  rest 
for  some  time,  and  then  administer  diuretics.  When 
diuretics  failed,  purgatives  rarely  succeeded.  He  had  not 
seen  benefit  from  the  use  of  the  hot  air  bath.  He  had 
entirely  failed  to  see  any  benefit  from  the  use  of  pilo- 
carpin.  Unlike  tapping  in  cirrhosis,  he  had  seen  but 
little  loss  of  strength  in  tapping  for  cardiac  dropsy.  He 
had  but  once  had  peritonitis  follow  tapping.  Southey's 
capillary  tubes  for  draining  the  legs  in  general  anasarca 
were  of  great  value,  although  he  had  seen  phlegmonous 
erysipelas  follow  their  use  in  one  case.  He  had  found 
that  diuretics  would  act  often  after  rest  and  good  diet, 
though  they  had  previously  failed. 

Dr.  Allbutt  had  found  diaphoretics  very  uncertain. 
He  regarded  hydragogues  as  very  useful.  The  air  bath 
was  unsuccessful.  He  hesitated  to  tap  the  patient's  leg 
in  fear  of  erysipelas,  but  otherwise  the  operation  was 
almost  brilHantly  successful.  He  used  Southey's  tubes 
with  satisfaction.  He  delayed  tapping  on  account  of 
the  exhaustion  it  produced. 

Dr.  Thomas  had  found  diaphoretics  inactive,  but  some- 


*  British  Med.  Association,  Aug.,  1882;  Med.  Record^  Aug.  26,  1882. 


TREATMENT   OF  VALVULAR  DISEASE.  21 5 

times  they  were  satisfactory  after  purgatives,  but  generally 
no  real  benefit  from  attempts  to  act  on  the  skin. 

Dr.  Carter  had  used  the  hot  air  baths  and  hot  drinks 
with  marked  benefit,  especially  in  dropsy  after  scarlet 
fever,  and  had  frequently  seen  diuresis  follow.  For 
cardiac  and  other  dropsies  digitalis  had  in  his  hands 
proved  to  be  exceedingly  useful.  He  had  resorted  to 
early  tapping,  but  he  had  used  a  very  small  trocar,  whi<:h 
would  allow  only  a  slow  removal  of  the  fluid,  believing 
that  thereby  the  liability  to  exhaustion  was  considerably 
diminished.  He  referred  to  three  cases.  The  first  was 
ascites  from  cirrhosis,  and  tapping  was  followed  by  gradual 
exhaustion.  The  second  was  ascites  with  Bright's  disease. 
In  this  tapping,  doubled  the  quantity  of  urine  and  was 
followed  by  relief.  The  third  was  ascites  with  cardiac 
disease,  and  each  tapping  was  followed  by  diminution  of 
the  urine  one  half,  although  relief  was  afforded.  The 
patient  was  tapped  seventeen  times.  The  patient  with 
cirrhosis  died,  the  other  two  left  the  hospital  in  a  com- 
paratively comfortable  condition.  He  had  used  Southey's 
tubes  for  the  legs  with  good  results.  He  believed  the 
use  of  hydragogues  should  not  be  constant,  but  occa- 
sional. He  preferred  rhubarb,  jalap,  etc.,  with  elaterium. 
Dr.  Roden  recommended  iodide  of  potassium  combined 
with  full  doses  of  nitric  acid.  Some  preparations  of  iron 
with  saline  cathartics  possessed  special  advantages. 

Dr.  Phillip's  had  used  Southey's  tubes  successfully,  but 
regarded  hypodermic  injections  of  pilocarpin  as  one  of 
the  most  valuable  agents  that  could  be  used. 


2l6  ANGINA  PECTORIS. 


LECTURE  XIV. 

ANGINA      PECTORIS 

Is  pretty  plainly  a  neuralgia.  Whether  the  change  that 
produces  it  is  in  the  muscle  of  heart,  caused  by  scanty 
supply  of  blood  to  the  organ,  or  is  in  the  terminal  branches 
of  the  cardiac  nerves,  or  as  the  Medical  Record'^  expresses 
it,  referring  to  Dr.  Allen  Sturge's  opinions,  due  to  "  a 
commotion  spontaneously  developed  in  the  gray  sub- 
stance of  the  sympathetic  ganglia  of  the  cardiac  plexus, 
this  being  transmitted  to  the  spinal  cord  and  brain;  a 
commotion  spontaneously  developed  in  the  cervical  sym- 
pathetic ganglia,  which  give  off  branches  to  the  cardiac 
plexus,  or  in  the  ganglia  of  the  vagus;  a  spontaneous 
commotion  in  the  part  of  the  gray  substance  of  the  cere- 
brum which  may  receive  impulses  coming  from  above 
and  below ;  or  to  a  spontaneous  commotion  in  the  parts 
of  the  gray  substance  of  the  cord  in  communication  with 
these  ganglia,  by  means  of  bands  of  nervous  substance 
passing  from  the  cord  to  the  great  sympathetic." 

Angina  arising  from  tobacco  is  a  rare  thing.  Tobacco 
causes  intermittence,  arythmia,  etc.  When  it  causes 
angina  it  is  due  to  the  slow  action  of  the  nicotine  on 
the  coronary  arteries. 

Angina  arising  from  alcohol  signifies  endarteritis  of  the 
coronary  arteries  as  well  as  degenerations  or  sclerosis  of 
the  myocardium.  The  mischief  is  done,  the  suppression 
will  not  avail. 

Gouty   angina  of    the    Germans    is    a   cardio-vascular 


*Med.  Rcc,  Sept.  22,  1883. 


ANGINA   PECTORIS.  217 

lesion  and  resists  treatment ;  it  is  like  alcoholic  angina 
caused  by  endarteritis  ;  the  alkalies  can  do  little  for  gout 
of  the  heart. 

Angina  of  organic  origin,  alterations  of  the  coronary- 
arteries,  degeneration  of  the  cardiac  muscle,  dilatation 
of  the  cavities,  and  lesions  of  the  aorta,  oftener  cause 
attacks  than  mitral  lesions. 

Hysterical  angina  is  very  rare.  These  neurotic  anginas 
are  nearly  as  dangerous  as  those  of  organic  origin. 

There  is,  in  fact,  no  paralysis  of  the  sympathetic  in 
angina  pectoris.  The  disease  is  in  reality  attended  by 
excitation  of  the  cardiac  sympathetic  nerves  and  coronary 
vessels ;  the  latter  being  in  a  state  of  erethism,  there  is  no 
paralysis  in  the  case  ;  but  there  is  not  even  excitation  of 
the  sympathetic  nerves,  accompanied  by  the  contraction 
of  the  blood-vessels  in  general,  the  disease,  so  far  as 
nerves  are  concerned,  being  partial  and  limited.  If  it 
were  possible  to  galvanize  the  cardiac  sympathetic  nerves, 
would  you  not  augment  rather  than  diminish  the  vaso- 
motor contractility? 

Obstruction  and  Regurgitant  Mitral  Murmur  with 
Healthy  Valve ;  also  Angina  Pectoris. — A  case  is  reported 
in  the  Lancet,  Jan.  27,  1883,  in  which  the  patient  died  in 
a  paroxysm  of  angina  pectoris,  left  hypertrophy  and  dila- 
tation and  the  mouths  of  the  coronary  arteries  obstructed. 
The  writer  believes  that  angina  pectoris  is  caused  by 
ischaemia  of  the  heart. 

The  patient  had  a  presystolic  and  a  systolic  murmur, 
yet  the  mitral  valve  was  normal  by  the  water  test  and  was 
perfectly  healthy  in  appearance.  The  presystolic  murmur 
had  in  this  case  its  usual  distinctive  feature — a  rough 
vibrating  quality  resembling  in  this  respect  the  sound 
produced  by  the  lips  when  thrown  into  vibrations  by  the 
expired  breath.     The  writer  calls  it  a  blubbering  sound. 

The  author  explains  the  murmurs  as  follows :  "  I  do 


2l8  _  ANGINA  PECTORIS. 

not  propose  to  discuss  the  various  explanations  of  the 
production  of  a  mitral  systolic  murmur  without  mitral 
lesion.  Suffice  it  to  say  that  in  this  case,  taking  into  view 
the  considerable  dilatation  of  the  left  ventricle,  it  seems 
to  me  probable  that,  although  the  ventricle  held  water 
when  filled  from  an  opening  made  through  the  apex, 
the  ventricular  contraction  during  life  occasioned  some 
regurgitation.  A  regurgitant  stream,  be  it  ever  so  small, 
may  give  rise  to  a  murmur.  I  submit  this  explanation 
without  undertaking  at  this  time  to  account  for  the  ap- 
parent incongruity  that  the  mitral  may  admit  of  some 
regurgitation  during  life  and  yet  be  found  competent 
after  death." 

Hysterical  Angina  Pectoris. — Marie*  reports  two  cases 
in  hysterical  patients.  In  one  the  pain  commenced  in  the 
left  little  finger,  ran  up  the  arm  to  the  breast  of  that 
side.  During  the  attack,  which  often  lasted  some  hours, 
the  pulse  of  the  left  radial  artery  became  imperceptible,  the 
lower  parts  and  the  whole  left  side  became  cold.  In  the 
second  case  the  attack  was  often  preceded  by  general 
malaise ;  then  a  sudden  violent  pain  in  the  prsecordial 
region  ;  accompanied  by  extreme  anguish,  invincible  ter- 
ror. The  pain  then  extended  towards  the  neck  and  left 
arm  and  little  finger,  and  sometimes  toward  the  leg.  The 
attack  lasted  ten  to  twenty  minutes,  and  the  face,  which 
was  at  first  pale  and  cold,  became  red  and  warmer.  He 
compares  them  to  a  form  of  angina  called  vaso-motor  by 
the  Germans,  but  does  not  say  whether  there  was  heart 
disease. 

Prof.  Sees  Treatment  of  the  Paroxysm, — See  has  aban- 
doned the  use  of  chloral.  It  induces  sleep,  but  has  no 
effect  on  the  circulation. 

Hypodermic    injection    of    morphine,  a   centigramme 

^-  *T\izM€d.  Rec,  June  2,  1883.         ■- 


ANGINA  PECTORIS.  219 

of  the  hydrochlorate,  one  sixth  of  a  grain,  may  be  re- 
peated, may  be  given  daily  to  prevent  return. 

Nitrite  of  amyl  is  one  of  the  most  active  and  useful 
means,  three  or  four  drops  inhaled  from  the  open  palm. 
In  the  first  period  of  the  action  the  vascular  tension  is 
lowered,  the  vessels  are  dilated,  the  action  of  the  heart  is 
very  much  quickened,  the  respiration  is  more  free  and 
easy.  At  a  more  advanced  period,  the  pressure  remain- 
ing lowered,  the  heart  and  respiration  become  slowed. 
There  is  sanguineous  irrigation  of  the  coronary  arteries, 
as  in  other  vessels,  the  cardiac  ischsemia  ceases.  From 
more  than  the  dose  indicated  there  is  risk  of  cardiac  syn- 
cope. The  patient  soon  becomes  accustomed  to  the  rem- 
edy, so  that  its  good  effects  become  less  and  less. 

Nitro-Glycerine. — The  effects  of  this  are  very  much 
like  those  of  the  nitrite  of  amyl,  only  slower.  The  dose 
is  one  or  two  drops  of  a  one  per  cent  solution. 

Sees  Treatment  in  the  Intervals. — Bromide  of  Potass- 
ium. Under  its  action  the  patient  becomes  less  impres- 
sionable to  physical  and  psychical  influences  which  might 
provoke  a  paroxysm,  but  it  produces  debility,  which  is 
more  or  less  permanent. 

Digitalis.  When  the  attacks  result  from  cardiac  atony 
or  degeneration  it  is  better  than  the  bromide ;  it  sustains 
the  action  of  the  heart  and  is  every  way  preferable. 

Of  electricity  he  speaks  very  doubtfully;  it  may  even 
kill,  as  in  Duchenne's  case. 

Angina  Pectoris  and  Counter  Irritation. — Dr.  W.  A. 
Sturge  *  explains  the  pectoral  pain  as  well  as  the  associ- 
ated dyspnoea,  gastric  disturbance,  brachial  soreness,  etc., 
by  the  conversion  of  an  efferent  impulse  conveyed  along 
certain  nerve  trunks  (the  cardiac  nerves)  into  a  general 
commotion  of  a  group  of  spinal  nerve  centers  with  which 

*  N.  Y.  Med.  Journal,  May  26,  1883. 


220  .  ANGINA  PECTORIS. 

these  trunks  are  connected,  and  by  the  consequent  in- 
volvement of  other  trunks  springing  from  the  same  cen. 
tres.  So  in  visceral  inflammations  he  believes  we  relieve 
pain  by  counter  irritation^  the  latter  exhausting  the  sen- 
sitiveness of  the  centre  which  supplies  nervous  force  both 
to  the  viscus  and  the  overlying  integuments,  so  that  by 
making  a  powerful  impression  on  the  latter  we  inhibit  the 
irritation  of  the  centre  upon  the  former. 

Nitrous  Compounds  in  Angina  Peetoris. — Dr.  Hay,* 
after  experimental  observations,  concludes  that  nitrous 
acid  in  any  combination,  whether  as  an  ether  or  metallic 
salt,  is  useful  in  the  treatment  of  angina  pectoris,  and 
that  in  the  case  of  the  nitrite  of  amyl  the  action  of  the 
acid  is  aided  by  that  of  the  base.  But  all  the  compounds 
of  nitric  acid  are  useless  unless  they  are  so  composed  that 
the  acid  is  converted  into  nitrous  acid  in  the  system.  So 
far  it  appears  that  nitrogen  containing  remedies  for  angina 
pectoris  may  be  divided  into  two  classes,  the  one  consist- 
ing of  combinations  of  nitrous  acid  with  metallic  oxides 
or  alcoholic  radicles,  the  other  comprising  a  peculiar  class 
of  nitric  ethers  obtained  from  higher  alcohols.  In  both 
classes  the  action  of  the  compound  is  ultimately  on  the 
nitrous  acid  present.  Examples  of  the  first  class  are  the 
nitrite  of  sodium,  and  the  nitrite  of  ethyl,  and  of  the  sec- 
ond class  nitro-glycerine.  Then  there  are  the  compounds 
of  amyl  whose  action  is  similar  to  that  of  nitrites.  But 
they  are  limited  at  present,  the  dose  required  is  large,  the 
action  is  not  rapidly  produced  ;  and  disagreeable  after 
effects  are  apt  to  be  produced.  They  are  not  to  be 
chosen  in  the  treatment  of  angina  pectoris. 

Nitro-Glycerine  is  a  vaso-motor  paralyzer  and  dilator  of 
the  peripheral  vessels,  and  is  of  service  in  diseases  of  the 
heart,  especially  those  of  the  aorta.  It  opposes  the  symp- 
— _______ — . — — _ « — , 

*  The  Medical  Record,  July  7,  1883. 


ANGINA   PECTORIS.  22 1 

toms  of  cerebral  anaemia,  as  Dujardin  Beaumetz*  has 
shown  to  be  the  case  with  the  nitrite  of  amyl.  In  cardiac 
affections  characterized  by  feeble  state  of  the  myocardium 
amyl  nitrite  has  been  regarded  as  a  cardiac  stimulus,  and 
nitro-glycerine  has  doubtless  the  same  action.  Nitro- 
glycerine has  been  especially  productive  of  good  results 
in  angina  pectoris  in  doses  of  three  drops  a  day  of  a  solu- 
tion of  one  to  a  hundred.  It  has  also  been  successfully 
used  in  tendency  to  syncope  and  in  palpitations,  but  only 
in  those  cases  in  which  there  is  a  nervous  or  anaemic 
state.  Free  diuresis  has  been  produced.  Formula :  Dis- 
tilled water,  fl  |  x,  solution  of  nitro-glycerine — i-ioo,  gr. 
XXX ;  three  teaspoonfuls  a  day,  one  after  each  meal. 

Angina  Pectoris  and Nitro-Glycerine. — Dr.  Jacob  Frankf 
of  Buffalo  treated  a  woman  aged  thirty-one  years  with 
morphine,  electricity,  etc.,  with  little  benefit.  He  then 
tried  nitro-glycerine  m.  j.  of  one  per  cent  solution,  grad- 
ually increased  m.  vj.  three  times  a  day  and  then 
decreased.  The  patient  had  no  more  of  the  disease. 
After  she  had  been  taking  the  medicine  for  six  weeks, 
aphthae  appeared  on  the  tongue,  mouth,  and  fauces.  The 
medicine  was  stopped,  and  these  ulcers  were  treated  with 
borax,  etc.,  after  which  the  treatment  was  resumed. 


*  Dr.  Henri  Huchard  Am.  Jour.  Med.  Science,  July,  1883. 
\  The  Medical  Record,  May  5,  1883. 


222  DEFORMITIES  OF  THE  HEART, 


LECTURE  XV. 

DEFORMITIES   OF  THE   HEART. 

Certain  congenital  malformations  of  the  heart  take 
place,  the  result  of  imperfect  foetal  evolution  ;  to  enter 
into  a  lengthy  discussion  of  these  conditions  would  in- 
volve an  extended  inquiry  into  the  science  of  embryology, 
which  is  not  intended.  The  principal  deformities  to 
which  the  organ  is  subject  may  be  briefly  summarized, 
as  arrests  of  development  during  some  period  of  intra- 
uterine existence,  in  which  the  heart  may  either  consist 
of  two  or  three  cavities :  those  in  which,  although  four 
cavities  exist,  there  is  a  deficiency  in  the  septa  between 
the  right  and  left  sides,  and  those  cases  in  which  the 
heart  is  not  confined  to  its  proper  cavity.  These  condi- 
tions may  be  best  elucidated  by  the  following  cases. 

Disease  of  Puhnonary  Valve  and  Open  Septum. — Dr. 
Bruen,*  in  the  Pathological  Society  of  Philadelphia,  de- 
scribes a  heart  thus :  Two  of  the  semilunar  leaflets  of  the 
pulmonary  artery  are  nearly  destroyed  by  atheromatous 
changes  ;  the  third  segment  is  much  thickened  and  pro- 
jects as  a  leaflike  fold,  roughening  the  mouth  of  the  pul- 
monary artery.  This  vessel  is  dilated  to  twice  its  natural 
size,  forming  nearly  an  aneurism.  The  vessel's  walls  are 
covered  with  vegetations  of  inflammatory  origin,  or  due 
to  atheromatous  changes.  The  right  auricle  is  very  small 
and  imperfectly  developed,  the  bulk  of  the  cavity  being 
formed  by  the  auricular  appendix.  The  tricuspid  valves 
are  much  thickened,  but  probably  competent.     Between 


*  Medical  Ne^vs,  Dec.  23,  1882. 


DEFORMITIES   OF  THE   HEART.  223 

the  ventricles  is  an  orifice  that  will  admit  the  forefinger. 
It  is  directly  beneath  one  of  the  tricuspid  leaflets  and  is 
lined  with  endocardium.  The  walls  of  the  right  ventricle 
are  thinned  and  its  cavity  somewhat  dilated.  Dr.  Bruen 
ascribed  the  perforation  to  the  pressure  of  blood  in  the 
right  ventricle.  The  dilated  artery  made  a  pulsating  tu- 
mor to  the  left  of  t^e  sternum,  between  the  second  and 
fourth  ribs.  Over  the  tumor  a  **  post  diastolic  and  presys- 
tolic bruit-like  murmur  could  be  heard,"  while  close  to 
the  junction  of  the  second  and  fourth  ribs  to  the  ster- 
num a  hoarse  systolic  murmur  could  be  heard.  There 
was  no  cyanosis. 

Dr.  Wilson  thought  that  in  this  case  the  left  heart  by 
its  greater  strength  had  sent  its  blood  into  the  right  and 
overloaded  it,  and  that  the  condition  of  the  pulmonary 
artery  was  due  to  this. 

Open  Ductus  Arteriosus. — Dr.  Beverly  Livingston*  re- 
ported to  the  N.  Y.  Pathological  Society  a  case  of  this 
kind.  In  a  newborn  male  child  there  was  no  indication 
of  disease  till  the  morning  of  the  third  day.  Then  there 
was  a  sudden  arrest  of  respiration ;  an  irregular  action 
of  the  heart,  cyanosis,  first  of  the  face,  then  of  the 
whole  surface  of  the  body.  In  a  minute  and  a  half  the 
pulse  resumed  its  regularity,  and  the  skin  its  natural 
color.  At  intervals  of  about  an  hour  the  same  symptoms 
recurred,  and  as  they  recurred  they  lasted  a  little  longer, 
about  two  minutes,  and  artificial  respiration  was  neces- 
sary for  the  restoration.  In  the  sixth  attack  the  best 
efforts  were  unavailing.  The  heart  ceased  beating  for- 
ever. 

The  lungs  showed  numerous  small  regions  of  collapse 
(atalectasis),  and  the  right  heart  was  distended  with 
blood. 

*Path.  Soc,  June  27,  1883. 


224  DEFORMITIES   OP  THE   HEART. 

Open  Foramen  Ovale. — Dr.  Ferguson  exhibited  at  a 
meeting  of  the  N.  Y.  Pathological  Society  two  hearts  il- 
lustrating persistent  foramen  ovale.  One  opening  admit- 
ted a  tube  half  an  inch  in  diameter.  Dr.  Allchin  of  Lon- 
don asked  Dr.  Ferguson  why  he  supposed  the  blood  in 
one  of  his  specimens  passed  from  one  auricle  to  the  other. 
He  had  seen  the  lesion  very  frequently,  and  supposed 
that  it  was  generally  accepted  that  the  pressure  of  the 
blood  in  both  cavities  was  so  nearly  equal  that  it  kept 
the  opening  sufficiently  closed  to  prevent  any  evidence 
that  the  blood  passed  from  one  auricle  to  the  other. 

Dr.  Ferguson  replied  that  the  arrangement  of  the  tis- 
sues was  such  in  one  of  the  cases  that  he  thought  pres- 
sure on  one  side  would  close  the  foramen,  and  that  pres- 
sure on  the  other  would  open  it. 

Ductus  Arteriosus  Open  in  a  Dog. — Dr.  W.  H.  Howell 
and  Professor  Donaldson*  found  in  a  dog  the  pulse  rate 
greater  and  the  cardiac  impulse  stronger  than  normal. 
The  apex  was  further  to  the  left  than  it  should  be,  show- 
ing marked  hypertrophy.  Over  all  the  cardiac  region 
Prof.  Donaldson  heard  a  loud  rasping  cardiac  murmur 
with  maximum  intensity  over  the  base,  also  a  slight 
murmur  with  the  second  sound.  Experiments  showed  a 
normal  arterial  pressure  and  no  abnormality  in  the  sphyg- 
mographic  tracings  except  an  unusually  marked  dicro- 
tism.  The  ductus  arteriosus  was  found  open,  its  calibre 
being  at  least  equal  to  that  of  either  of  the  pulmonary 
arteries.  With  such  free  communication  between  the 
aortic  and  pulmonary  circulation  it  is  noticeable  that  so 
good  an  average  arterial  pressure  was  maintained  (as  meas- 
ured in  the  femoral  artery).  Only  one  such  case  is  found 
on  record. 

I  have  not  the  **  circular"  in  which  this  account  was 


*  N.  Y.  Med.  Jour.,  March  3,  1883. 


DEFORMITIES   OF   THE   HEART.  *       22  5 

first  published,  but  this  abstract,  as  I  suppose  it  is, 
leaves  the  impression  that  "  the  loud  rasping  mur- 
mur" was  produced  by  blood  flowing  through  the  open 
ductus  arteriosus.  But  there  is  no  reason  to  suppose 
that  the  ductus  arteriosus  produces  any  more  noise  when 
the  blood  passes  through  it  than  does  the  aorta,  or  the 
carotid  where  it  divides  into  internal  and  external.  It  is 
easy  enough  to  hear  the  sounds  of  the  heart  in  utero,  yet 
'*  a  loud  rasping  murmur''  is  almost  never  heard.  The 
report  does  not  mention  the  aortic  valves. 

Then  the  blood  pressure  was  apparently  taken  in  the 
femoral  artery,  where  it  would  represent  the  strength  of 
the  left  ventricle,  and  a  good  part  of  that  of  the  right, 
and  until  the  heart  became  enfeebled,  the  pressure  ought 
to  be  considerable,  at  least  compared  with  that  in  the 
carotid  artery. 

Congenital  Communication  between  the  Right  Side  of  the 
Heart  and  the  Aorta.—Dr.  B.  Livingston*  exhibited  to  the 
N.  Y.  Pathological  Society  the  heart  of  a  child,  a  male 
three  months  and  twenty  seven  days  old,  that  had  been 
strong  and  healthy,  and  had  never  given  any  symptom  of 
heart  disease.     He  died  of  entero-colitis. 

Thymus  gland  large ;  heart  enlarged  ;  at  root  of  the 
aorta  on  the  right  side  was  a  communication  with  the 
right  heart.  ''Above  and  below  the  tricuspid  valve  it 
was  closed  by  a  part  of  this  valve,  and  most  Hkely  no 
blood  passed  through  it."  The  valves  of  the  aorta  were 
only  two  in  number,  but  were  sufificient  to  close  the 
opening.  The  mitral  and  tricuspid  valves  were  normal. 
On  the  mitral  were  plenty  of  those  semi-transparent 
nodules  referred  to  in  other  cases. 

Congenital  Pulmonary    Stenosis. — Dr.    B.    Livingstonf 

*  Med.  Record,  Sept.  i,  1883. 
flbid. 


226  DEFORMITIES   OF   THE   HEART, 

reported  to  the  N.  Y.  Pathological  Society  an  instance  cfi 
this  obstruction  that  occurred  in  a  female  child  one  year 
and  eight  months  old.  The  parents  believed  that  the  dis- 
ease existed  at  birth.  When  Dr.  Livingston  first  saw  her 
she  was  pale,  not  cyanotic,  short  of  breath,  disposed  to 
rest.  A  systolic  very  loud  murmur  was  heard  most  dis- 
tinctly at  the  union  of  the  fourth  left  rib  with  the  sternum, 
and  nearly  as  distinctly  at  apex ;  was  also  heard  in  sixth 
intercostal  space  to  left  of  apex  beat  and  between  the 
scapulae.  There  was  a  distinct  fremitus  over  the  prse- 
cordia4  region  felt  by  the  hand.  She  died  of  septicaemia 
following  mild  ulcerative  stomatitis. 

"The  three  semilunar  valves  of  the  pulmonary  artery 
had  grown  together,  so  as  to  leave  a  round  hole  two 
millimetres  in  diameter,  and  on  one  side  there  was  a  small 
vegetation,  which  must  have  been  an  obstacle  to  the  cur- 
rent of  blood.  The  foramen  of  Botal  was  enlarged  and 
open,  and  the  interauricular  septum  was  very  much 
thinned,  and  there  were  some  small  holes  through  it,  so 
that  it  had  a  cribriform  appearance."  The  heart  was 
hypertrophied  and  the  left  side  dilated. 

Stenosis  and  Atresia  of  the  Piilmonary  Artery  and 
Opening  in  the  Ventricular  Septuin."^ — A  boy  of  thirteen 
years.  He  was  under  observation  about  four  and  a  half 
months.  In  the  boy's  opinion  and  memory  he  had  been 
cyanotic  from  four  years  of  age  (probably  from  both). 
He  had  attacks  of  deep  cyanosis  lasting  some  days, 
during  which  he  would  become  wholly  or  partly  uncon- 
scious, the  respiration  slow  and  sighing,  the  pulse  rapid 
and  feeble,  120  to  150,  the  pupils  widely  dilated  and  insen- 
sible to  light ;  the  temperature  at  first  somewhat  elevated, 
100°  to  102°,  but  later  it  would  fall  slightly  below  the 
standard,  while  the  extremities  would  be  cold  and  covered 


*  Dr.  B.  A.  Watson,  N.   V.  Path.  Soc.  Med.  Record,  March  10,  1883. 


DEFORMITIES   OF  THE   HEART.  22; 

by  a  slight  perspiration.  These  attacks  were  generally 
produced  by  slight  fatigue,  or  exposure  to  the  sun  (it 
was  in  summer)  and  were  always  preceded  by  several 
hours  with  severe  headache  and  a  general  feeling  of  illness. 
He  died  in  such  an  attack  in  which  for  the  first  time  he 
complained  of  a  severe  pain  in  the  praecordial  region. 

Two  murmurs  were  heard  at  the  base  and  two  at  the 
apex.  During  the  attacks  only,  subscrepitant  rales  were 
heard  over  the  whole  chest. 

The  heart  was  found  to  be  large  ;  the  left  auricle  was 
only  half  the  capacity  of  the  right ;  the  tricuspid  and 
mitral  valves  were  healthy.  Two  segments  of  the  aortic 
valve  were  sealed  together  by  a  material  of  cartilagin- 
ous firmness  ;  the  valve  was  atheromatous  and  covered 
with  vegetations.  There  was  marked  stenosis  of  the 
pulmonary  valve.  There  was  an  opening  through  the 
ventricular  septum  which  permitted  the  little  finger  to 
pass  through  it  easily.  The  left  carotid  artery  arose  from 
the  innominata  and  the  left  subclavian  nearer  the 
median  line  than  usual.  It  is  not  probable  that  there 
were  two  murmurs  at  the  apex  distinct  from  those  at  the 
base,  but  it  is  probable  that  the  base  murmurs  were  con- 
ducted so  strongly  as  to  deceive  the  observer.  It  seems 
that  no  murmur  was  recognized  that  could  be  referred  to 
the  opening  in  the  septum. 

Dr.  Eskridge  exhibited,  at  the  meeting  of  the  Patholo- 
gical Society  of  Philadelphia,  March  3,  1883,  an  unusual 
deformity  of  the  aorta  and  the  aortic  valve.  The  speci- 
men was  taken  from  a  man  about  seventy  years  of  age, 
who  had  suffered  a  number  of  years  from  severe  heart 
disease.  The  walls  of  the  large  arteries  were  thickened, 
rigid  and  contained  numerous  deposits  of  inorganic  mat- 
ter. The  left  ventricle  was  enormously  enlarged.  The 
first  half  inch  of  the  aorta  was  hard  and  unyielding  from 
fibrous  thickening' and  calcification.     Each  section  of  the 


228  DEFORMITIES  OF  THE   HEART. 

valve  was  almost  wholly  transformed  into  a  bone-like 
matter,  and  at  points  the  valves  were  a  quarter  of  an  inch 
in  thickness.  They  were  immovable  and  almost  entirely 
closed  the  opening.  ''One  of  the  leaflets,  about  three 
fourths  of  an  inch  in  all  directions,  with  its  vegetations 
stretched  across  the  aorta,  lay  against,  and  was  apparently 
adherent  to  the  other  segments  of  the  valve,  the  latter 
being  curled  upon  themselves.  The  central  portion  of 
the  aorta  was  entirely  occluded,  and  only  two  small  open- 
ings remained"  between  the  segments  of  this  valve  near 
the  artery  : — one  three  m.  m.  by  one,  the  other  about  two 
thirds  this  size.  Then  other  similar  openings  had  existed, 
but  were  obliterated  before  death  by  a  thin  fibrous  trans- 
parent membrane.  The  valves  on  the  aortic  side  were 
very  rough,  but  on  cardiac  side  were  rather  smooth.  A 
vegetation  ten  m.  m.  long  was  attached  to  one  of  the 
segments.  One  segment  was  adherent  to  aorta  for  about 
half  an  inch,  while  the  free  portion  was  folded  on  itself 
and  pointed  toward  the  orifice. 

Dr.  H.  Horace  Grant*  reports  the  case  of  a  mulatto  girl 
aged  i6,  who  was  poorly  developed,  had  never  menstru- 
ated, had  often  coughed  up  blood,  had  remarkable 
clubbed  fingers  and  toes,  had  a  great  deal  of  dyspnoea, 
had  a  loud  tricuspid  regurgitant  murmur,  and  increased 
praecordial  dulness.  Her  ill-health  was  traced  back  to 
her  birth.  Her  complexion  forbade  the  recognition  of 
cyanosis. 

The  right  auricle  was  greatly  dilated,  the  right  ventricle 
moderately,  the  tricuspid  valve  was  insufficient.  There 
was  no  pulmonary  artery.  The  aorta  was  given  off  just 
above  the  septum,  one  half  from  the  left  ventricle  and 
one  half  from  the  right.  The  three  sections  of  the  aortic 
valve  arose,  one  on  the  right,  one  on  the  left  of  the  aorta, 


Am.  Jour,  of  Med,  Sci.,  July,  1883. 


DEFORMITIES   OF  THE   HEART.  229 

and  the  third,  posterior,  from  the  top  of  the  septum. 
The  two  coronary  arteries  arose  from  the  right  sinus  of 
Valsalva.  The  puhnonary  arteries  were  given  off  from 
the  front  of  the  aorta  at  the  pericardial  attachment  each 
about  half  an  inch  in  diameter. 

Sundrifold  Pulmonary  Valve, — A  young  man  20  years 
of  age  died  from  fracture  of  the  skull  caused  by  a  fall 
down  a  flight  of  stairs  when  intoxicated.  The  valves  of 
the  pulmonary  artery  were  tested  by  water  and  were 
found  slightly  incompetent.  There  were  four  valves  (or 
cusps) ;  three  of  about  the  ordinary  size,  the  fourth  much 
smaller  than  the  others,  and  imperfectly  separated  from 
one  of  them.  The  other  valves  of  the  heart  were  healthy, 
and  the  heart  was  of  natural  size. 

He  had  been  examined  by  Dr.  Begbie  repeatedly  dur- 
ing the  three  years  preceding  his  death.  A  very  decided 
thrill  and  a  loud  blowing  murmur  attended  the  systole  at 
the  left  border  of  the  sternum  at  the  third  rib.  The 
thrill  was  very  limited.  The  murmur  was  diffused  over 
the  upper  part  of  the  chest,  but  was  scarcely  appreciable 
in  the  carotids.  There  was  a  much  fainter  diastolic  mur- 
mur almost  limited  to  the  same  spot.  (Begbie's  Works, 
Sydenham.) 

Double  Ventricle  and  Insufficient  Septum. — Mr.  Stone, 
in  St.  Thomas's  Hospital  Reports,*  gives  the  following : 
Heart  not  excessively  large,  the  vessels  given  off  nor- 
mally. Ductus  arteriosus  closed;  water  injected  by  the 
aorta  comes  out  freely  by  the  pulmonary  artery.  The 
finger  passed  into  the  pulmonary  artery  meets  obstruc- 
tion an  inch  and  a  half  below  the  valve.  The  auricles 
communicated  by  a  slit-like  fissure  such  as  is  not  uncom- 
mon without  producing  any  pathological  effect.  The 
walls  of  the  right  ventricle  were  hypertrophied  to  exactly 

*  Am.  Jour,  of  Med.  Sci.,  Oct.,  1883. 


230  DEFORMITIES   OF  THE   HEART. 

an  equal  in  thickness  to  those  of  the  left.  The  cavity  of 
the  ventricle  was  divided  into  two  chambers,  one  much 
smaller  than  the  other,  and  almost  completely  shut  off 
from  it  by  a  firm  fleshy  partition.  These  were  in  com- 
munication with  each  other  by  a  small  circular  aperture 
with  cartilaginous  margin,  studded  with  vegetations  of  the 
size  of  a  millet  seed,  about  a  quarter  of  an  inch  in  diame- 
ter. The  small  oval  chamber  was  an  inch  and  a  half  long, 
situated  between  the  general  cavity  and  the  pulmonary 
valve.  This  was  quite  healthy.  The  septum  between 
the  ventricles  was  perforated  by  a  large  semilunar  orifice 
in  its  upper  space. 

During  life  there  was  a  distinct  systolic  thrill  over  the 
cardiac  region,  most  marked  at  a  part  half  way  between 
the  left  mamma  and  the  sternum,  and  conveyed  upward 
in  a  diagonal  line  from  the  midsternal  toward  the  outer 
extremity  of  the  left  clavicle.  This  was  accompanied  by 
a  loud,  rough  sound,  also  systolic,  most  accentuated  at  the 
point  covering  the  origin  of  the  pulmonary  artery.  It 
was  not  loud  at  the  apex  of  the  heart,  was  also  lost  to 
the  right  of  .the  sternum,  but  was  audible  over  the  up- 
per part  of  the»scapula  posteriorly,  and  less  distinct  lower 
down.  The  heart  was  somewhat  enlarged  toward  the 
left  side.  '*  The  pulmonary  valve  was  healthy,"  and  as 
nothing  is  said  of  the  other  valves  it  is  wrong  to  infer 
that  they  were  healthy  also.  The  thrill  and  rough  sound 
must  have  been  produced  at  "  the  small  circular  aper- 
ture." 

No  Aortic  Orifice. — Dr.  Alfred  Meyer*  reports  the  fol- 
lowing case  :  A  male  infant  twenty-four  days  old,  cyanotic 
all  over  the  body,  suffering  great  dyspnoea,  no  radial  pulse 
on  either  side,  distinct  pulse  in  the  dorsalis  pedis,  135. 
Nothing  abnormal  was  found  in  the  lungs,  but  there  was 

*  The  Med.  Record,  April  21,  1883. 


DEFORMITIES   OF   THE   HEART.  23 1 

a  loud,  distinct  blowing  systolic  murmur  in  the  neighbor- 
hood of  the  second  and  third  ribs  to  the  right  of  the 
sternum.  The  mother  said  he  had  been  short  of  breath 
from  his  birth,  but  that  the  skin  was  not  discolored  till 
the  third  week.  The  gradual  increase  of  the  dyspnoea 
while  nursing  and  the  deepening  cyanosis  alarmed  her. 
The  child  was  found'  dead  in  bed  forty-eight  hours  later. 

The  pericardium  contained  three  fourths  of  a  drachm 
of  clear  serum  ;  heart  substance  of  dark  blue  color.  The 
right  auricle  and  ventricle  greatly  dilated;  foramen  ovale 
pervious ;  pulmonary  artery  fully  twice  its  normal  size ; 
ductus  asteriosus  pervious  ;  left  auricle  one  third  the 
size  of  the  right  ;  walls  of  the  left  ventricle  half  an  inch 
thick;  its  cavity  just  large  enough  to  hold  a  small  pea; 
pectinean  muscles  fused  into  a  solid  mass  ;  mere  traces  of 
the  chordae  tendineae.  Aortic  orifice  completely  closed ; 
dictus  arteriosus  leads  into  the  arch  of  the  aorta,  which 
is  about  one  eighth  of  an  inch  in  diameter  and  ends  in  a 
blind  sac  at  the  base  of  the  heart.  The  septum  ventric- 
ulorum  complete. 

This  patient  lived  twenty-seven  days.  Two  other  re- 
corded cases  give  a  life  of  two  and  four  days  respectively. 

Atresia  and  stenosis  of  the  aorta  at  or  above  the  open- 
ing of  the  ductus  arteriosus  is  comparatively  common. 
Eppinger  collected  42  cases  and  adds  2  of  his  own. 
The  patient  may  live  50  or  60  years  ;  one  lived  to  92. 

Both  Septa  of  Heart  Deficient. — Dr.  H.  A.  Gallatin*  re- 
cords the  case  of  a  male  infant  thirty  months  old,  in 
whom  the  heart  was  as  large  as  that  of  an  adult  female, 
the  increase  almost  wholly  in  the  right  cavities,  the  auricle 
and  ventricle  having  each  a  capacity  of  two  ounces,  and 
the  walls  of  the  latter  were  half  an  inch  thick ;  a  probe 
passed  through  the  valves  of  the  pulmonary  artery  appeared 

*The  Medical  Record,  Oct.  20,  1883. 


232  DEFORMITIES   OF  THE  HEART 

in  the  aorta.  There  was  an  opening  in  the  ventricular 
septum  at  the  top  three  quarters  of  an  inch  in  diameter, 
so  that  the  aorta  and  pulmonary  artery  both  communi- 
cated freely  with  either  ventricle,  or  with  both,  most 
freely  with  the  right.  The  semilunar  valves  of  the  aorta 
and  pulmonary  artery  were,  however,  perfect.  The  fora- 
men ovale  was  open  three  quarters  of  an  inch.  The 
Eustachean  valve  had  disappeared. 

The  patient  was  tall  and  delicate,  upper  parts  of  the 
body  usually  cedematous,  subject  to  turns  of  cyanosis,  and 
even  fainting;  surface  cold  and  patient  chilly;  there  was 
dyspnoea  by  turns.  Varying  murmurs  not  constant;  the 
most  constant  was  a  presystolic  rippling  sound. 

A  Diverticulum,  or  Glove-Finger  Extension  of  the  Left 
Ventricle. — Dr.  Gilbert*  records  the  case  of  an  infant  who 
lived  to  the  age  of  ten  months  in  whom  was  a  ventral 
hernia  and  defective  abdominal  wall  in  the  middle  line 
from  the  umbilicus  upward.  The  diaphragm  was  found 
to  be  defective  also,  so  that  the  pericardium  opened  into 
the  abdominal  cavity ;  and  projecting  into  the  abdomen 
was  a  pouch-like  diverticulum  attached  to  the  apex  of  the 
left  ventricle,  with  muscular  walls  and  having  internally 
fleshy  columns  like  the  ventricular  cavity  itself.  This  ap- 
pendix was  thirty-eight  millimetres  in  length,  and  shaped 
like  the  finger  of  a  glove.  Dr.  Peacock  in  his  "  Malforma- 
tions of  the  Heart,"  though  he  refers  to  several  cases  of 
defect  of  the  pericardium,  does  not  mention  any  such 
abnormality. 

Dextro-cardiUy  the  other  Viscera  in  their  Proper  Places. — 
Dr.  D.  Frank  Sydstonf  reports  the  case  of  a  man  twenty- 
four  years  of  age,  a  barber.  He  says  :  "  The  heart  occupies 
precisely  the   same   relation    on   the   right   side  that  it 


*  Med.  Record^  Aug.  ii,  1883. 
\  Ibid.,  July  21,  1883. 


DEFORMITIES   OF   THE   HEART.  ^  233 

ordinarily  does  on  the  left,  the  apex  being  in  the  right 
fifth  intercostal  space."  Otherwise  the  heart  appears  to  be 
perfectly  healthy.  "  The  abdominal  viscera  are  in  their 
normal  positions,  a  point  to  which  especial  attention  is 
directed,  inasmuch  as  such  cases  are  usually  accompanied 
by  a  transposition  of  the  liver  and  spleen."  He  refers  to 
the  pathological  displacements  of  the  heart  of  which  this 
is  not  one,  as  he  has  none,  and  has  had  none  of  the  diseases 
which  cause  such  displacement.  He  calls  it,  therefore, 
"An  instance  of  a  quite  rare  anomaly,  congenital  dextro- 
cardia. 

Open  Foramen  Ovale;  Perforated  Septum  Ventriculorum. 
— Reported  by  Dr.  Toupet.*  A  child,  seven  years  old, 
had  had  measles  and  whooping  cough ;  cyanosis  from  birth, 
blue,  temperature,  96.5°;  eyes  prominent;  nails  enormous- 
ly hypertrophied ;  heart  very  large  ;  respiration  rapid  and 
labored ;  at  the  level  of  the  third  costal  cartilage,  near 
the  left  border  of  the  sternum  a  loud  blowing  systolic 
sound.  On  inspection  the  heart  lay  nearly  in  the  median 
line  owing  to  the  greater  size  of  right  ventricle,  right 
auricle  normal,  but  left  rudimentary  ;  aorta  greatly  dilated 
up  to  the  origin  of  the  left  subclavian  artery,  beyond 
that,  normal.  The  pulmonary  artery  only  one  fourth  the 
size  of  the  aorta ;  the  walls  of  the  right  ventricle  very 
thick,  tricuspid  valve  healthy ;  the  infundibulum  separated 
by  a  partition  from  the  right  cavity,  which  was  pierced  by 
an  opening  of  the  size  of  a  small  goose  quill ;  the  mitral 
valve  was  normal;  in  the  upper  part  of  the  ventricular 
septum  was  a  hole  that  admitted  a  finger;  the  aorta  arose 
exactly  at  the  septum,  communicating  with  both  ventricles ; 
valve  of  the  foramen  ovale  was  not  adherent  and  was 
pierced  by  two  openings  of  the  size  of  a  crow-quill ;  the 
lungs  were  congested. 

*  Med.  Record,  Aug.  4,  1883. 


234  DEFORMITIES    OF   THE   HEART. 

Malformation  {?)  Aortic. — Dr.  Thomas  B.  Peacock*  gives 
the  following  description  of  the  condition  of  a  heart  and 
thinks  the  lesion  was  congenital.  "The  right  and  posterior 
segments  of  the  aortic  valve  were  blended  together  so 
that  the  aortic  opening  had  but  two  valves ;  both  of  them 
were  very  much  thickened,  and  the  under  curtain  fell 
below  the  level  of  the  other  curtain,  so  that  there  was 
obstruction  and  regurgitation.  • 

The  action  of  the  heart  was  tumultuous  and  visible 
over  a  large  space ;  there  was  decided  prominence  in  the 
praecordial  region.  Dulness  on  percussion  began  in  the 
second  interspace  and  became  entire  in  the  third. 
Laterally  it  begins  to  the  right  of  the  sternum  and 
extends  beyond  the  line  of  the  left  nipple.  At  the  base 
there  was  a  systolic  murmur  heard  most  distinctly  at  the 
right  side  and  upper  part  of  the  sternum ;  it  was  short 
and  rough  and  followed  by  a  soft  diastolic  murmur  which 
was  propagated  down  the  course  of  the  sternum.  Toward 
the  apex  there  was  a  creaky  murmur  which  was  independ- 
ent and  perhaps  presystolic,  not  heard  posteriorly.  Per- 
haps a  slight  passing  tremor  felt  at  the  apex. 

Ectopia  Cordis. — M.  Tarnierf  exhibited  at  a  meeting 
of  the  Academic  de  Medicin  a  woman  whose  sternum 
was  bifurcated  at  the  lower  part,  so  that  the  beating  of 
the  heart  could  be  seen  to  take  place  immediately  under 
the  skin  of  the  epigastric  region.  The  ventricular  part 
could  be  seized  between  the  fingers ;  by  palpation  over 
the  upper  part  of  the  notch  the  contractions  of  the 
auricles  could  be  detected.  Apparently  the  diaphragm 
did  not  exist  under  the  heart.  M.  Beau  believed  that 
the  beat  of  the  heart  was  due  to  dilatation  under  the 
influence    of   the   afflux   of   blood   at    the   time   of   the 


\  Am.  Jour,  of  Med.  Sci.,  Oct.,  1883. 
*  The  Medical  Record,  Oct.  6,  1883. 


FUNCTIONAL   DISEASES   OF   THE   HEART.  235 

ventricular  systole.  According  to  him  the  apex  of  the 
heart  contracts  during  the  diastole.  In  this  case  it  was 
easy  to  perceive  that  the  ventricle  was  soft  during 
diastole,  and  hard  during  the  systole.  In  systole  the 
apex  of  the  heart  struck  the  thoracic  wall. 


LECTURE   XVL 

FUNCTIONAL  DISEASES   OF  THE   HEART. 

Forced  Heart. — There  is  a  diseased  condition  of  the 
heart  observed  for  the  most  part  in  those  who  have  made 
great  and  prolonged  physical  exertion,  whether  in  violent 
games,  heavy  labor,  climbing  ladders,  running  matches  or 
forced  marches,  heavy  drills,  and  the  like,  which  has  been 
called  "the  overwrought  heart,"  "the  forced  heart,"  the 
irritable  heart. 

This  condition  most  physicians  have  seen,  and  perhaps 
have  not  distinguished  it  from  irritable  heart  arising  from 
other  causes.  It  has  been  described  in  France  and 
Germany,  and  in  England  by  Maclean  and  Myers.  Cases 
have  been  seen  in  fifties  abroad,  but  as  our  war  brought 
into  conflict  a  greater  number  of  men  than  were  ever 
mustered  into  the  field  before,  the  medical  muster 
should  be  correspondingly  large.  Dr.  Da  Costa  alone, 
in  a  military  hospital  under  his  charge,  saw  more  than 
three  hundred  cases.  He  had  the  means,  therefore,  of 
giving,  and  probably  has  given,  the  best  description  of 
the  disease  which  we  possess.  It  may  be  found  in  the 
Am.  Jour,  of  Med.  Set.,  Jan.,  1871.  I  also  had  large 
numbers  of  army  patients  in  the  years  of  the  war.     But 

as  Bellevue  Hospital  stands  on  the  river,  and  the  helpless 


236  FUNCTIONAL  DISEASES   OF   THE  HEART. 

cases  had  to  be  carried  on  stretchers  only  about  two 
hundred  feet,  they  were  all  landed  there,  while  the  walk- 
ing cases  were  sent  to  hospitals  more  distant  from  the 
river.  These  cases  of  irritable  heart  are  almost  all  walk- 
ing cases,  and  therefore  passed  by  us  to  the  upper 
hospitals. 

I  am  not  ignorant  of  this  disorder,  but  am  about  as 
familiar  with  rupture  of  the  valves  or  heart  wall  from 
strain  as  with  the  "overworked  heart."  It  is  wise  then 
to  take  the  portraiture  of  the  disease  from  Dr.  Da  Costa, 
whose  opportunity  of  studying  it  has  so  far  excelled  that 
of  anybody  else. 

Dr.  Da  Costa  says  in  substance  that  a  soldier  in  active 
duty  is  debilitated  by  a  diarrhoea  or  fever,  but  soon  cured, 
returns  to  duty,  but  finds  that  as  he  exerts  himself  he  gets 
out  of  breath,  and  falls  behind  his  comrades  in  the  march  ; 
has  dizziness  and  palpitations  of  the  heart,  and  pain  in, 
the  chest.  He  is  oppressed  by  his  gun  and  knapsack. 
At  the  hospital  his  rapid  pulse  proves  his  infirmity, 
although  he  looks  like  a  man  in  sound  health.  Any 
associated  disorders  may  soon  pass  away,  but  the  irri- 
tability of  the  heart,  the  excited  organ  only  slowly  return- 
ing to  its  healthy  action,  or  the  excitement  may  continue 
till  the  patient  is  discharged  from  the  army  or  is  sent  to 
the  invalid  corps. 

There  are,  he  says,  many  others  in  whom  the  irregularity 
of  the  heart's  action  and  pain  in  the  region  of  the  heart 
occur  more  suddenly  without  previous  disease. 

Dr.  Da  Costa  describes  the  symptoms,  and  says  that 
in  those  not  having  organic  disease  of  the  heart  they 
were  as  follows : 

Palpitatiojis. — In  some  the  attacks  lasted  many  hours. 
They  occurred  at  all  hours  of  the  day  or  night,  and  were 
repeated  in  some  six  or  more,  in  others  occurring  but 
once  in  twenty-four  hours,  while  some  were  free  from 


FUNCTIONAL  DISEASES   OF  THE   HEART.  237 

them  for  days.  Sometimes  the  attacks  were  so  violent 
as  to  produce  unconsciousness,  while  physical  exertion 
was  a  uniform  cause  of  palpitation  ;  they  occurred  also 
when  the  patient  was  in  bed  and  even  asleep.  Some 
were  worse  at  night  and  early  morning.  The  attacks 
were  accompanied  by  cardiac  uneasiness  and  pain,  and 
pain  under  the  left  shoulder  and  in  some  by  headache, 
dimness  of  vision,  and  giddiness.  With  some  exceptions 
the  patients  would  not  lie  on  the  left  side  in  bed,  fearing 
that  that  position  would  provoke  an  attack.  But  there 
were  some  who  preferred  the  left  decubitus,  and  somd 
who  could  lie  on  either  side  or  on  the  back. 

Pain. — This  was  almost  a  constant  symptom,  varying 
in  character  from  a  dull  ache  to  sharp  and  lancinating. 
In  a  few  it  was  a  burning  sensation,  or  tearing.  Some- 
times it  preceded  the  palpitations,  and  sometimes  oc- 
curred without  them.  In  rare  instances  it  was  relieved 
hy  muscular  exertion,  but  was  generally  caused  by  it. 
Deep  breathing  in  some  increased  the  severity  of  the 
pain. 

The  chief  seat  of  the  pain  was  over  the  heart  near  its 
apex ;  it  was  also  felt  above  the  inferior  angle  of  the  left 
scapula,  in  the  left  axilla,  and  down  the  left  arm,  attended 
there  with  numbness.  Sometimes  it  radiated  from  the 
heart  in  every  direction.  With  the  pain  there  was  hyper- 
aesthesia  in  the  cardiac  region.  The  pain,  the  author 
thinks,  was  not  an  intercostal  neuralgia,  but  that  affection 
sometimes  occurred  as  a  complication. 

Pulse  was  generally  very  rapid — 100  to  140 — small  and 
compressible.  It  might  or  might  not  have  the  jerky 
character  of  the  heart  beat,  and  was  subject  to  great  vari- 
ations. It  was  noticed  the  change  in  frequency  was  greatly 
affected  by  change  of  position.  In  one  case,  the  patient 
standing,  it  was  105  to  108,  after  lying  down  less  than  80, 
and  fuller,  in  another  it  changed  from  124  to  94.    These 


238  FUNCTIONAL  DISEASES   OF  THE   HEART. 

pulse  records  were  made  during  the  absence  of  palpita- 
tions ;  during  these  the  frequency  was  increased.  The 
author  also  observed  a  frequent  tendency  to  cyano- 
sis. 

Respiration. — Respiratory  oppression  on  exertion  and 
in  the  palpitations  was  constant ;  a  little  of  it  was  felt  at 
all  times,  and  there  were  occasions  when  the  patient 
could  not  lie  down.  The  normal  ratio  of  the  breathing 
and  heart  beats  was  quite  broken  up.  A  man  with  a 
pulse  at  124  breathed  25  times  a  minute,  one  with  a  pulse 
at  146  breathed  26  times,  and  one  whose  pulse  beat  192 
times  breathed  26  times. 

Nervous  Disorders. — The  headache  was  constant  as  a 
symptom,  or  in  duration.  It  is  most  likely  to  follow  se- 
vere palpitations.  Dizziness  was  not  uncommon.  It 
was  increased  by  exercise  and  -stooping  ;  often  preceded 
the  palpitations,  and  in  one  case  at  least  caused  a  fall 
from  a  horse.  Disturbed  sleep,  jerkings  in  sleep,  and 
frightful  dreams  were  not  uncommon. 

Itchings  of  the  skin  and  excessive  perspirations,  or  of 
the  hand  only,  were  complained  of  by  several. 

Digestive  Disorders^  with  "irritable  heart,"  indigestion, 
abdominal  distention,  and  diarrhoea  are  very  common, 
but  Dr.  Da  Costa  regards  them  as  more  connected  with 
the  cause  of  the  disease  than  a  consequence  of  it. 

The  Urine  contained  oxalate  of  lime  and  other  products 
of  impaired  digestion  sometimes,  but  never  anything  that 
was  peculiar  to  this  affection. 

Physical  Examination. — The  beat  of  the  heart  was 
quick,  and  not  remarkably  strong,  often  irregularity  of 
rhythm.  The  first  sound  of  the  heart  is  feeble  and  short, 
resembling  the  second  in  duration.  The  second  sound  is 
sometimes  increased,  always  distinct.  Sometimes,  he 
says,  "  the  sounds  of  the  heart  are  split,"  "  there  were 
double  beats  and  intermissions." 


FUNCTIONAL  DISEASES   OF  THE  HEART.  239 

The  disease,  for  the  most  part,  either  slowly  subsided 
or  was  followed  by  degrees,  by  enlargement. 

Dr.  Da  Costa,  referring  to  causes,  has  constructed  the 
following  table,  showing  its  relation  to  fevers  and  diarrhoea. 
The  symptoms  did  not  generally  appear  till  the  patients 
were  sent  back  to  duty. 

200  CASES.  p.  c. 

Fevers \ , 17. 

Diarrhoea 30.5 

Hard  Field  Service 38, 5 

Wounds,  Injuries,   Rheumatism,  Scurvy,  Soldier  Life, 
and  Doubtful 18. 

100. 

He  has  another  table  in  which  the  '^  results"  are  shown 
in  200  cases,  and  in  which  death  finds  no  place. 

Treatment. — In  Dr.  Da  Costa's  remedies  rest  has  the 
first  place — rest  in  bed,  not  only  at  night,  but  for  many 
hours  of  the  day.  His  most  esteemed  drug  is  digitalis. 
He  gives  the  next  place  to  veratrum  viride.  Aconite 
found  but  little  favor  with  him ;  gelsemium  none  at 
all.  Belladonna  corrected  the  irregularities  of  the  heart, 
but  did  not  reduce  the  frequent  beat.  Opium  he  used 
only  for  the  diarrhoea  and  severe  pain,  but  he  decHned  to 
use  it  against  the  irritability,  fearing  that  in  a  long  use  of 
it  he  would  establish  the  opium  "  habit."  Hyoscyamus 
while  not  valueless,  was  not  much  praised.  Conium,  can- 
nabis indica,  valerian,  ergot,  and  the  bromides  did  not 
win  his  confidence  to  any  great  degree. 

Tonics  were  often  valuable,  and  zinc  had  some  control 
over  the  disease.     Iron  was  valuable  in  the  anaemic  cases. 

Dr.  Da  Costa's  paper  is  one  of  the  most  valuable  of  the 
age.     It  is  a  structure  built  by  square  and  plurnmet. 

Heart  Sympathies. — The  heart  bounds  with  joy,  it  sinks 
in  great  disappointments,  at  sights  of  horror.  Some 
persons  faint  at  the  sight  of  blood.  Fear  does  not  often 
paralyze  the  heart,  as  it  often  does  the  muscular  strength, 


240  FUNCTIONAL  DISEASES  OF  THE  HEART. 

but  it  causes  rapid  and  small  pulse,  while  it  contracts  the 
capillaries  of  the  surface  and  brings  paleness  and  nervous 
tremors  or  large  shakings.  A  gentleman  was  brought  to 
me  by  the  physician  of  a  life  insurance  company  for 
my  opinion  as  to  the  freedom  of  his  lungs  from  phthisis. 
On  the  first  examination,  for  some  reason,  now  forgotten, 
I  was  not  willing  to  answer  the  question :  should  the  risk 
be  taken  ?  On  a  second  examination,  I  answered  affirma- 
tively. This  fixed  the  gentleman's  attention  strongly  on 
this  liability  to  consumption.  Two  or  three  months 
afterward  a  messenger  summoned  me  to  visit  him  at  once. 
I  replied,  "  Call  his  physician"  (the  late  Dr.  Van  Buren). 
The  messenger  soon  returned  stating  that  Dr.  Van  Buren 
was  not  at  home  and  urged  that  I  must  go  at  once.  It 
was  raining  a  deluge,  but  I  waded  to  the  gentleman's 
house.  He  was  on  a  sofa,  was  as  pale,  or  rather  white, 
as  the  pillow  on  which  his  head  rested ;  his  movements 
were  as  tremulous  as  if  he  had  the  ''  shaking  palsy." 
His  pulse  was  small  and  rapid.  His  voice  was  low  and 
on  a  monotone.  I  asked  what  had  happened.  He 
said 'he  had  been  raising  blood.  I  asked  him,  How 
much  ?  An  attendant  raised  and  unfolded  a  handkerchief 
which  had  on  it  numerous  stains  of  blood.  The  blood 
had  spread  into  and  was  diffused  in  the  threads  of  the 
cloth,  not  in  coagulated  masses  with  slight  diffusion,  as 
blood  from  the  lungs  would  be.  It  was  blood  that  was 
mingled  with  the  saliva,  which  had  delayed  its  coagulation. 
I  asked  him  if  he  had  hurt  his  tongue  while  at  dinner. 
He  did  not  know  that  he  had.  I  asked  for  a  candle.  His 
wife  brought  it  in  a  hand  trembling  hardly  less  than  her 
husband's.  I  found  a  laceration,  a  penetrating  wound  in 
the  left  side  and  back  part  of  the  tongue,  as  if  a  wood- 
splinter  or  the  fragment  of  a  nail  from  a  flour  barrel 
had  been  forced  by  a  molar  tooth  into  the  tongue.  I 
informed  him  of  my  discovery,  and  then  he  remembered 


FUNCTIONAL   DISEASES   OF  THE   HEART.  24I 

that  he  did  have  a  pain  in  the  tongue  while  at  dinner. 
But  when  he  was  informed  that  the  blood  came  from  the 
tongue  and  not  from  the  lungs,  he  exclaimed :  *'  Why, 
wife,  I  feel  better.  Why,  I  can  sit  up,  I  can  stand  up, 
I  can  walk,"  which  he  did  then  and  there  across  the 
floor.  I  returned  through  the  rain  to  my  dinner  and 
heard  no  more  from. my  patient.  The  load  of  fear  lifted 
from  his  heart,  it  resumed  its  natural  mode  of  working, 
and  the  vaso-motor  nerves  relaxed  their  grasp  on  the 
capillaries. 

Cardiac  Neurasthenia!^ — In  some  cases  of  exhaustion 
from  continuous  over-work,  the  symptoms  centre  chiefly 
about  the  heart.  The  symptoms  are  feeble  cardiac  action, 
giddiness,  weakness,  intermittent  beat.  There  may  be 
palpitations,  dyspnoea,  and  even  syncope.  A  physician 
who  suffered  in  this  way  writes  that  he  was  relieved 
entirely  by  the  following  prescription : 

3  Quin  sulphate gr.  xxiv. 

Mist  camph ad.  §  vj. 

Acid  hydrobromic  dil 3  iij> 

Tinct  digital §  ss. 

Liq.  aurant §  j. 

Tinct.  Nuc  vom 3  ij. 

M.  Half  an  ounce  three  times  a  day. 

Cardiac  Typhoid, — Mr.  Bernheimf  designates  by  this 
term  cases  in  which,  without  notable  organic  alteration 
of,  without  pulmonary  complication,  or  others  capable  of 
explaining  the  occurrence,  the  pulse  becomes  small,  fre- 
quent and  depressed.  The  patient  succumbs  to  this  para- 
lytic acceleration  of  the  heart,  which  may  occur  at  the 
beginning  of  the  fever,  with  or  without  concomitant 
nervous  adynamia  or  at  a  more  or  less  advanced  stage  of 
it.    The  temperature  may  be  moderately  febrile,  normal  or 

*  The  Medical  Record,  Jan.  20,  1883. 
f  Ibid.,  Jan.  20,  1883. 


242     EFFECTS  OF  CERTAIN  DRUGS   ON   THE  HEART. 

subnormal.  He  considers  this  nervous  asystole  in  typhoid 
fever  to  be  due  to  the  direct  action  of  the  poison  on  the 
cardiac  innervation.  The  author  bases  his  conclusions  on 
six  cases  with  autopsies.  They  ended  in  sudden  death 
and  no  alteration  of  the  heart  correspondent. 

Cardiac  Vertigo^  I  cannot  say  I  am  very  familiar 
with,  aside  from  that  faintness  which  may  attend  grave 
aortic  obstructions  and  regurgitations.  The^  Medical  Rec- 
ord, however,  quotes  Germain  See  as  saying  that  when  it 
occurs  in  the  course  of  heart  disease,  we  need  to  look  no 
further  for  its  cause,  as  a  rule ;  that  in  cases  of  troublesome 
vertigo  the  heart  should  always  be  examined  for  its  cause, 
especially  if  extreme  pallor,  a  prominent  symptom  of 
aortic  insufficiency,  be  present,  and  will  not  yield  to  med- 
ication. .  .  In  these  cases  there  are  also  the  characteristic 
pains  of  angina  pectoris,  coming  on  every  few  months — 
another  prominent,  though  not  constant,  symptom  of 
aortic  incompetency. 


LECTURE    XVII. 

THE  EFFECTS  OF  CERTAIN  DRUGS  ON  THE  HEART. 

Accidents  Caused  by  Tobacco. — Vallinf  has  lately  re- 
ported to  the  Societe  de  Medicine  Publique  some  cases 
of  poisoning  by  tobacco  in  smokers  that  are  very 
emphatic.  In  M.  Vallin's  cases  symptoms  akin  to  those 
of  angina  pectoris  were  produced.  Indeed,  he  calls 
the  affection  angina  pectoris.  Take  a  case.  It  is  a 
"young  lieutenant  of  vigorous  constitution  who  for  a 
year  had  been  subject  to  attacks  of  angina  pectoris.     The 

*  Med.  i?<?(r.,  Sept.  22,  1883. 

\  Annates  de  Hygiene  Publique,  April,  1883. 


EFFECTS  OF  CERTAIN  DRUGS  ON  THE  HEART.     243 

attacks,  at  first  rare,  had  become  more  frequent — indeed, 
almost  daily.  The  day  after  his  admission  to  the  hospi- 
tal I  witnessed  an  attack — atrocious  retro-sternal  pains, 
with  painful  engorgement  of  the  left  side  of  the  neck, 
extreme  anguish,  paleness  of  the  face,  cold  sweat,  a  ten- 
dency to  fainting,  respiration  deep  and  sighing,  a  marked 
slowness  of  the  pulse,  fifty-two  pulsations  with  irregular- 
ity and  intermittence.  This  state  of  praecordial  anxiety 
continued  about  twenty  minutes.  The  patient  often  said 
he  was  about  to  die.  At  length  the  pains  ceased ;  the 
face  regained  its  usual  color.  There  remained  a  ten- 
dency to  vertigo  when  he  was  in  the  erect  position,  which 
continued  for  half  an  hour  more."  This  young  man  had 
been  admonished  that  he  must  stop  smoking,  and  he  had 
adopted  the  advice,  but  his  friends  assembled  in  his  room 
every  evening,  and  smoked  from  eight  to  eleven  o'clock. 
M.  Vallin  informed  the  patient  that  he  could  as  well  be 
poisoned  by  the  smoke  of  others  as  by  his  own.  He  ap- 
preciated this  information,  and  from  the  next  day  these 
attacks  grew  milder,  and  after  ten  days  there  were  none 
that  were  at  all  marked,  and  M.  Vallin  adds :  "  I  have  rea- 
son to  believe  that  the  suppression  of  the  cause  led  to 
the  definite  suppression  of  the  attacks." 

Another  case  follows  in  which  there  was  great  dizziness 
and  tendency  to  faint,  a  slow  pulse,  twenty-four  a  minute, 
with  intermittent  pulse  and  arrest  of  the  heart  beats,  ring- 
ing in  the  ears.  The  attacks  were  preceded  and  accom- 
panied by  extreme  praecordial  anxiety  without  localized 
pains,  but  with  suffocation  and  dyspnoea.  The  syncopal 
attack  recurred  about  every  two  hours.  The  patient  had 
had  rheumatism,  and  M.  Vallin,  though  there  was  no 
murmur  or  enlargement,  could  not  but  believe  that 
these  symptoms  were  the  result  of  rheumatic  changes  in 
or  on  the  heart  till  he  learned  that  the  patient  had  been 
a  great  smoker.      Abstinence  from  tobacco  had  nearly 


244     EFFECTS  OF  CERTAIN  DRUGS  ON  THE   HEART. 

effected  a  cure  when  M.  Vallin,  wishing  to  confirm  his 
second  diagnosis,  allowed  his  patient  a  pretty  strong 
segar.  When  he  had  smoked  one  half  of  it  he  was  at- 
tacked with  great  praecordial  anguish,  a  tendency  to  faint. 
He  was  obliged  to  go  to  bed,  and  to  keep  the  horizontal 
position,  and  this  time  had  great  frequency  of  pulse.  The 
same  experiment  was  tried  once  more  in  a  more  advanced 
stage  of  convalescence  with  the  same  results,  and  this 
time  there  was  great  slowness  of  the  pulse,  and  then  fol- 
lowed great  weakness  of  the  legs,  so  that  he  could  not 
walk  for  a  week.  His  recovery,  however,  was  complete 
in  the  end. 

A  physician  makes  his  third  case.  This  person  smoked 
excessively.  He  had  from  time  to  time  pretty  strong  inti- 
mations that  this  excess  was  injuring  him.  Nature 
seemed  to  assume  the  office  of  monitor  by  causing  an 
absolute  disgust  for  tobacco  of  several  days'  duration  ;  still 
he  smoked  when  he  could  and  all  he  could,  till  symptoms 
of  angina  pectoris  fully  alarmed  him.  He  then  stopped 
smoking  and  got  well. 

M.  Vallin  refers  to  a  dozen  cases  reported  to  the  Acad- 
emic des  Sciences  by  M.  Decaisne  of  intermittence  of  the 
heart  and  pulse  caused  by  the  abuse  of  tobacco.  Also 
to  a  sort  of  epidemic  of  angina  pectoris  which  occurred 
among  sailors.  There  was  a  great  tempest.  They  were 
confined  in  a  very  small  apartment  in  which  all  ventila- 
tion was  prevented  to  keep  out  the  sea.  They  smoked 
excessively  in  this  confined  air.  The  men  were  attacked 
— the  report  does  not  state  in  what  time — with  this 
disorder  both  those  who  smoked  and  those  who  did  not. 
This  disorder  ceased  in  a  little  time  after  by  the  suppres- 
sion of  tobacco.  Some  members  of  the  society  related 
analogous  cases. 

M.  Vallin  believes,  and  probably  truly,  that  excessive 
smokers  get  at  length  a  saturation  of  nicotine,  and  then 


EFFECTS  OF  CERTAIN  DRUGS  ON  THE  HEART.  245 

a  Spark  will  set  off  the  magazine,  a  slight  cause  will  pro- 
duce alarming  symptoms,  and  that  this  susceptibility  will 
last  six  months  to  two  years. 

Bad  Effects  of  Nitrous  Oxide  on  the  Heart. — Dr.  Ottley* 
observed  the  following :  A  young  woman  who  had  suf- 
fered from  rheumatic  fever  which  had  left  a  slight  mitral 
lesion,  with  a  faint  murmur,  sometimes  hard  to  hear,  and 
a  little  enlargement  of  the  heart,  but  no  functional  dis- 
turbances, took  the  gas  for  the  extraction  of  a  tooth. 
Nothing  important  followed.  A  few  days  later  she  took 
it  again,  and  so  much  dyspnoea  and  cardiac  irregularity 
was  caused  that  the  administration  of  the  gas  had  to  be 
suspended.  Subsequently  the  patient  suffered  from  pal- 
pitation and  dyspnoea,  the  heart  acted  irregularly,  and 
the  murmur  was  very  much  louder.  The  heart  now  for 
the  first  time  gave  evidences  of  inadequacy.  The  case  is 
interesting  from  its  rarity,  the  gas  having  been  given  in- 
discriminately with  surprisingly  few  accidents. 

Action  of  Digit alin  on  the  Heart. — Experiments  on  ter- 
rapins and  frogs  by  Drs.  H.  H.  Donaldson  and  M.  War- 
field.f  They  say  when  the  heart  is  doing  normal  work 
digitalin  decreases  that  work ;  that  there  is  a  rough  relation- 
ship between  the  size  of  the  dose  and  the  extent  of  the 
decrease  ;  that  with  small  doses  the  pulse  rate  is  at  first  in- 
creased ;  that  the  diminution  of  the  heart's  work  is  much 
more  dependent  on  the  strength  of  the  dose  at  any  given 
time  than  on  the  total  amount  of  the  drug  administered. 
A  large  amount  given  in  several  hours  has  much  less  effect 
than  a  smaller  amount  given  in  a  few  minutes.  There- 
fore, the  theory  that  digitalin  has  a  cumulative  action 
lacks  experimental  confirmation. 

Action  of  Alcohol  on  the  Heart. — Prof.  Martinij:  of  the 

*  N.  Y.  Med.  Jour.,  June  16,  1883. 
f  Ibid.,  March  3,  1883. 
X  Ibid.,  Oct.  13,  1883. 


246     EFFECTS   OF  CERTAIN  DRUGS   ON  THE   HEART. 

Johns  Hopkins  University  has  found  that  alcohol  in 
quantity  not  directly  poisonous  did  not  affect  the  rate  of 
the  pulsation.  Blood  containing  one  eighth  per  cent  by 
volume  of  absolute  alcohol  did  not  affect  the  amount  of 
work  done.  Blood  containing  one  fourth  per  cent  always 
diminished  it,  and  might  so  reduce  the  amount  sent  out 
by  the  left  ventricle  that  it  was  not  sufficient  to  supply 
the  coronary  arteries.  (About  0.46  of  an  ounce  of  alco- 
hol for  a  man  of  150  pounds.) 

Alcohol,  in  Prof.  Martin's  opinion,  does  not  act  on  the 
heart  tiJl  it  reaches  the  muscular  and  nervous  tissues 
through  the  coronary  arteries. 

As  alcoholic  blood  holds  its  oxygen  more  firmly  than 
other  blood,  it  is  probable  that  the  deleterious  action  of 
alcohol  is  due  to  the  deprivation  of  oxygen  which  it 
causes  in  the  tissues.  . 


INDEX. 


Acute  pericarditis,  serous  efifusion 
in,  41 

Adhesion,  pericardial,  41 

Adonis  vernalis,  206 

Alcohol,  effect  of,  245 

Anaemic  murmurs.  Graves  on,  20 

Angina  pectoris,  216 

"       alcohol  as  a  cause  of,  216 

'*       amyl  nitrite  in,  219 

"       chloral  in,  218 

**       counter  irritation  in,  219 

"       digitalis  in,  219 

'•       electricity  in,  219 

"      gouty,  216 

**       hysterical,  217 

"       hysterical,  cases  of,  218 

'*       nitro-glycerine  in,  219 

**       nitrous  compounds  in,  220 

'*      morphine  in,  218 

**       of  organic  origin,  217 

'*       potassium  bromide  in,  219 

**       pathology  of,  216 

"       tobacco  as  a  cause  of,  216 

*'      treatment  in  the  intervals, 

219 
"      treatment  of  the  paroxysm, 
218 

Aortic  disease,  179 

"      malformation,  234 
'*      obstruction,  181 
'*     obstructive  murmur,  13 
**     orifice,  absence  of,  230 
*'     regurgitant  murmur,  13 
"     regurgitation,  pulse  of,  185 
**  "  second  sound 

abolished  in,  193 

Asynchronism,  29 

"  from  anaemia,  29 

**  from  asphyxia,  29 


Atheroma,  163 

"  pathological     changes 

in,  164 
Auscultatory  percussion,  33 

Balfour  on  anaemic  murmurs,  18 
Blood,  course  of,  through  heart,  10 
Block  on  opening  the  pericardium, 

Bony  deposit  in  heart,  184 
Bruit,  cause  of,  11 

"     de  diable,  18 

**     de  fluctuation y  94 

**     de  la  toupie,  18 

"     de  pot  feld,  94 

"     de  rape,  12 

"     trumpet,  196 

Cactus  grandiflorus,  213 
Calcification  of  pericardium,  75 
Cardiac  and  renal  disease,  198 

disease,  iron  in,  206 

dilatation,  Niemeyeron,  132- 

disease,  treatment  of,  206 

irregularities,  29 

movements,        interference 
with  by  adhesions,  42 

neurasthenia,  241 

oedema   resulting  from  en- 
docarditis, 168 

typhoid,  241 

typhoid  fever,  121 

vertigo,  242 
Carditis  secondary  to  pericarditis, 

46 
Cook  on  double  heart  beat,  27 
Convallaria  majalis,  209 
Coronary     arteries,     anastomoses 
of,  32 


248 


INDEX. 


Cors  hovinum,  123 

Deformities  of  the  heart,  222 
Deformity  of  heart,  227,  228 
Degeneration,  adipose,  142 

*'  fatty,  recognition  of, 

143 
'*  fibrous,  156 

"  pathology  of  fibrous, 

156 
"  Quain's,  142 

"  Quain's,  bicarbonate 

of  soda  in,  147 
**  Quain's,  case  of,  145 

**  Quain's,    causes     of, 

146 
'*  Quain's,   diet  in,  147 

**  Quain's,       frequency 

of,  146 
**  Quain's,.      pathology 

of,  144 
*'  Quain's,       treatment 

of,  146 
Depressor  nerve,  31 
Dextro-cardia,  232 
Diastolic  sound,  14 
Differentiation   of  exo-  and  endo- 
cardial sounds,  47 
Digitalin,  effect  of,  245 
Digitalis,  212 

"       infusion  of,  64 
Dilatation,  aneurismal,  of  heart,  190 
."  bleeding  in,  140 

*'  causes  of,  132 

"      "    136 
**  diagnosis  of,  137 

**  frequency  of  simple,  137 

**  King  on,  16 

**  of  heart,  132 

**  Peabody  on,  133 

**  physical  signs  of,  137 

"  rational  signs  of,  138 

"  simple,  136 

**  strychnia  in,  141 

"  treatment  of,  140 

Direct  murmurs,  13 
Diseases  of  heart,  formula  for  de- 
tection of  valvular,  15 
Disease,  valvular,  of  right  side  of 

heart,  detection  of,  16 
Double  heart  beat,  26 

"       "  explanation  of,  28 
Dropsy,  caffein  in  cardiac,  206 
**      cardiac,  Leech  on  treatment 
of,  214 


Drugs,  effects  of,  on  heart,  242 
Ductus   arteriosus,    case  of  open, 

223,  224 
Dyspnoea,  causes  of,  139 

Ectopia  cordis,  234 

Effusion,  position  of  pericardial,  40 

Endocarditis,  96 

"  and  hepatic  abscess, 

III 
**  diagnosis  of,  104 

*'  embolism  in,  102 

'*  extent  of,  100 

**  in  pysemia,  ill 

**  in    rheumatic    fever, 

108 
"  Kuchler  on  foetal,  193 

••  mechanism  of  valvu- 

lar deformity  from, 
103 
**  murmurs  in,  106 

"  pathology  of,  loi 

**  post  mortem  appear- 

ances of,  no 
"  prognosis  of,  105 

**  statistics  of,  148 

"  temperature  curve  of, 

III 
**  thickening   of  valves 

from,  102 
**  treatment  of,  ill 

"  ulcerative,  112 

lOI 

"  •*  results  of, 

112 

**  vegetations  from,  103 

Endocardium,  9 
Embolism,  statistics  of,  149 
Extra-cardiac  ganglia,  30 

Fatty  degeneration,  142 

**  **  varieties    of, 

142 
Fibrous  degeneration,  156 
Fibroid  induration,  190 
Fleshy  columns,  10 
Foramen  ovale,  open,  224 
"      233 
Forced  heart,  235 

"  "      pathology  of,  235 

'•  '*     symptoms  of,  236,  et. 

seq. 
*'  "      treatment  of,  239 

Francis  on  heart  scanning,  26 


INDEX. 


249 


Functional    defangement, 

regurgitation  from,  213 
Functional  diseases,  235 


mitral 


Graves  on  anaemic  murmurs,  20 

HyEMOTO-PERICARDIUM,  94 

Heart,  bony  deposit  in,  i66,  184 
Heart  clot,  159 

"  colors  of,  160 

**  diagnosis  of  ante-  and 

post-mortem,  159 
"  pathology  of,  i6i 

**  when  formed,  159 

Heart,  congenital  opening  between 
right  side  of,  and  aorta, 
225 
*'       deformities  of  the,  222 
**      disease  of,  due  to  rupture 

of  tendinous  cords,  14 
*'       disease  of  right  side  of,  14 
**      disease,  effect  of,  on  cardiac 

nerves,  186 
"      hypertrophy  of,  122 
*'      intra-uterine  disease  of,  14 
**     largest  reported,  133 
*'      nerves  of,  29 
"      position  of  normal,  39 
**      puncture  and  suture  of,  89 
**      Roberts  on  puncture  of,  89 
"      Westbrook  on  puncture  of, 

89 
**      rupture  of,  150 
"  **  from      myocar- 

ditis, 150 
**      scanning,  26 
**      sounds,  9 
*'      suture  of,  155 
"      sympathies,  239 
Hypertrophy,  122 

"  and  palpitation,  131 

**  and  pleurisy,  129 

**  causes  of,  125 

"  concentric,  122 

"  definition  of,  122 

**  diagnosis  of,  128 

"  eccentric,  122 

"  from  anger,  125 

"  from  contracted  kid- 

ney, 126 
*•  from  sexual  ejJcess, 

126 
•*  from  valvular  lesions 

125 
"  pathology  of,  123 


Hypertrophy,  physical  signs  •f,  128 
"  possible    extent    of, 

123 
**  rational  signs  of,  130 

**  simple,  122 

**  with  dilatation,  122 

Indirect  murmurs,  13 
Intra-cardiac  ganglia,  30 
Isham  on  the  sphygmograph,  25 

Jugular  pulsation,  178 

Keyt    on    transmission    of   pulse 

wave,  25 
King  on  dilatation  without  injury, 

16 
Kuchler  on  foetal  endocarditis,  193 

Leech  bites,  results  of  enormous 

haemorrhage  from,  71 
Leech    on    treatment    of    cardiac 

dropsy,  214 

Micrococci,  114 

Mitral    obstruction,    consequences 
of,  191 
**      regurgitation  from  functional 

derangement,  213 
"      stenosis,  194 
**  "         prognosis  of,  192 

*'      valve,  15 
Murmurs,  anaemic,  17,  18 

Balfour  on,  18 
**         constant  diastolic,  100 
'*         designation  of,  17 
**         differential  diagnosis  of 
intra-  and  peri-cardial, 
20 
'*         in  chlorosis,  18 
**         tones  of,  17 
**         lying  in,  196 
**        organic,     disappearance 

of,  17 
**         pericardial,  20-21 
**        presystolic,  12 
"         tones  of,  12 
Myocarditis,  116 

*'  cardiac   aneurism  in, 

118 
causes  of,  120 
consequences  of,  120 
effusion  in,  117 
embolism  in,  117 
heart  failure  from,  I2X 


250 


INDEX. 


Myocarditis,  pathology,  ii6 
"  repair  after,  117 

*'  rupture  in,  ti8 

"  symptoms  of,  117 

**  symptoms  of,  120 

Nerves  of  heart,  29 

Niemeyer  on  cardiac  dilatation,  132 

Nitrous  oxide,  effects  of,  245 

Obstruction,  murmur  of,  11 
CEdema  of  valves,  104 
Opium  in  uremia,  67 

Partzersky  on  drainage  of  peri- 
cardium, 92 
Peabody  on  dilatation,  133 
Pepper's  case  of  tapping  the  peri- 
cardium, 82 
Percussion,  new  method  of,  34 
Pericardial  adhesion,  41 

"  adhesions,   Gibson  on, 

88 

"  adhesions,  signs  of,  85 

"  drainage,  90 

"  effusion,  40 

**  effusions,  encysted,  43 

**  incision,  90 

**  friction  sound,  47 

**  friction,  disappearance 

of,  51 
**  friction  sound,  double, 

47 
*'  friction    sound;    when 

heard,  47 
Pericarditis,  32 

"  alkalies  in,  60 

"  amount  of  effusion  in, 

54 
**  bleaching  in,  63 

**  blisters  in,  66 

"  cancer   of  oesophagus 

producing,  92 
**  causes  of,  44 

"  citrate  of  potash  in,  64 

•*  clinical  history  of,  55 

**  connected  with   gran- 

ular kidney,  44 
**  diagnosis  of,  50  et  seq. 

**  digitalis  in,  64 

"  dry,  47 

"  following    erysipelas, 

44 
•*  following  haemor- 

rhage, 44 


Pericarditis,  following     malignant 
disease,  44 
following  pleurisy,  44 
following  pneumonia, 

44 
following  r  h  e  u  m  a  - 

tism,  44 
following    scarlatina, 

44 

from    contiguous    in- 
flammation, 45 

generally    secondary, 

44 
haemorrhagic,  40 
mercury  in,  59 
morbid  anatomy  of,  39 
occurrence    in    pneu- 
monia, 57 
occurring  in  pyaemia, 

45 
opium  in,  66 
peculiar  case  of,  77 
physical  diagnosis  of, 

i6 
prevention  of  by  dia- 
phoresis, 65 
prognosis  of,  56 
salicylic  acid  in,  61 
sero-purulent  effusion 

in,  44 
sometimes  primary,44 
symptoms  of,  46 
tonics  in,  66 
treatment  of  59 
walking  case  of,  55 
Pericardium,  aspiration  of,  82 

Block  on  opening  the, 

90 
calcification  of,  75 
indications    for    tap- 
ping, the,  80 
mode  of  puncture  of, 

82 
Pepper's  case  of  tap- 
ping the,  82 
point  of  puncture  of, 

81 
Roberts    on   tapping 

the,  81 
structure  of,  32 
tapping  of;  recovery, 

84 
tapping  the,  80 
Pleurisy  and  heart  disease,  192 
Pneumo-pericardium,  92 


INDEX. 


251 


Pneumo-pericardium,  causes  of,  92 

**  signs  of,  93 

Pulmonary  valve,  sundrifold,  229 
Pulse-wave,  rapidity  of   transmis- 
sion of,  25 

Regurgitation,  murmur  of,  11 

**  without       ^valvular 

disease,  13 
Right  ventricle,  penetrating  the,  91 
Roberts  on  puncture  of  heart,  89 
'*        on  tapping  the  pericardi- 
um, 81 
Rosenstein   on    pericardial  drain- 
age, 90 
Rupture  of  the  heart,  150 

**         **    •      "       causes  of,  151 
"      from   myo- 
carditis, 1 50 

Salicyl  compounds,  213 
Salicylate  of  soda,  objections  to,  63 
Salter  on  cardiac  rhythm,  26 
Scabrous  effusion,  41 
Scarification,  use  of,  73 
Second  sound,  accentuated,  23 
**  **      exaggerated  in  ane- 

urism, 23 
Septa,  both  cardiac,  deficient,  231 
Septum,  open,  with  disease  of  pul- 
monary valve,  222 
Sibson  on  pericardial  adhesions,  88 
Sounds  of  heart,  accentuated,  23 
'*         "        cause  of,  21 
**         **        mechanism  of,  22 
Solid  stethoscope,  34 
Sphygmograph,  24 

**  compound,  24 

Stenosis,   congenital,    pulmonary, 
225 
**        of  right  auriculo-ventric- 

lar  opening,  193 
'*        relative,  197 
Suture  of  heart,  155 


Thrombosis,  cardiac,  in  acute  dis- 
ease, 161 
Tobacco,  effects  of,  242  et  seq 
Tonsilitis,  murmurs  in,  109 
Tricuspid   insufficiency,  191 

"  stenosis,  194 

'*  valve,  14 

Valves,  injuries  to,  153-154 

"  "       of  heart,  position 

of,  96 
**      pulmonary,    diagnosis     of 

disease  of,  183 
"       rupture  of,  172 
**       structure  of,  9 
Valvular  disease,  163 

**         "  causes  of,  160 

**         "  endocarditis     as 

cause  of,  170 
**        "  general       effects 

of,  175 
"         **  of  right  side,  183 

**         **  pathology  of,  174 

**         **  prognosis  of,  204 

**         **  relation    of    kid- 

ney disease  to, 
182 
**        lesions,  duration  of,  179 
**        stenosis,  173 
Vaso-motor  nerves,  effect  of  action 

of,  31 
Venesection,  69 
Ventricle,  diverticulum  of,  232 

'*         double,  with  insufficient 

septum,  229 
**        perforation  of  by  gastric 
ulcer,  155 
Ventricular    septum,  opening    in, 
with  atresia,  226 

Wet  cups,  use  of,  73 
West  on  pericardial  drainage,  90 
Westbrook    on    puncture    of    the 
heart,  89 


